ED Emergency Management Tool
46 conditions · Full drug doses · NICE / RCEM / BTS / RCOG guidelines · For qualified ED clinicians
NICE UK 2024–25 · RCEM · BTS · RCOG · ReviseMRCEMALS — Cardiac Arrest
Resuscitation Council UK 2021 · Shockable & non-shockable · Post-ROSC care
RCUK 2021Call crash team. Start CPR: 30 compressions : 2 breaths. Rate 100–120/min. Depth 5–6 cm. Minimise interruptions. Rotate compressors every 2 min.
- 1Confirm VF / pVT on monitor. Call for defibrillator. Continue CPR until charged.
- 21st shock: Biphasic 150–200 J (or per manufacturer). Resume CPR immediately × 2 min without pulse check.
- 3Establish IV/IO access during CPR. Airway: supraglottic/ETT — do not interrupt for >5 sec.
- 42nd shock: 150–360 J. Resume CPR × 2 min.
- 53rd shock: Give Adrenaline 1 mg IV + Amiodarone 300 mg IV immediately after shock. CPR × 2 min.
- 6Continue: shock every 2 min. Adrenaline every alternate loop (every ~3–5 min). 2nd amiodarone 150 mg after 5th shock.
- 7Treat reversible causes continuously — see 4Hs & 4Ts below.
Capnography target during CPR: ETCO₂ >10 mmHg suggests adequate compressions. Sudden rise in ETCO₂ may indicate ROSC.
- 1Confirm PEA or asystole — check gain, leads, contact. Do NOT shock.
- 2Start CPR. Establish IV/IO access as soon as possible.
- 3Adrenaline 1 mg IV/IO as soon as access obtained.
- 4Continue 2-min CPR cycles. Adrenaline every 3–5 min (every alternate loop).
- 5Actively identify and treat reversible causes (4Hs & 4Ts) — this is the key intervention.
- 6Consider echo (POCUS) for reversible structural causes (tamponade, PE, massive MI).
- Hypoxia → ensure airway, oxygenate
- Hypovolaemia → IV fluid / blood bolus
- Hypo/Hyperkalaemia, metabolic → ABG, electrolytes, glucose
- Hypothermia → warm IV fluids, active rewarming
- Tension pneumothorax → needle decompression 2nd ICS MCL
- Tamponade → pericardiocentesis (USS guided)
- Thrombosis (PE/STEMI) → thrombolyse or primary PCI
- Toxins → antidotes, gastric lavage
- 112-lead ECG immediately — STEMI or ≥2 contiguous ST changes → activate cardiac cath lab urgently
- 2Target SpO₂ 94–98% (PaO₂ 10–13 kPa). Avoid hyperoxia — titrate FiO₂ down.
- 3Target PaCO₂ 4.5–5.0 kPa — avoid hyperventilation (worsens cerebral perfusion)
- 4Target MAP ≥65 mmHg, SBP ≥100 mmHg. Vasopressors as below.
- 5Blood glucose: target 6–10 mmol/L. Avoid hypoglycaemia.
- 6Targeted Temperature Management (TTM): target 36°C × 24h for comatose survivors
- 7CT head ± CT coronary angiography. Transfer to ICU.
- 8Neuroprognostication: not before 72h post-ROSC (or 72h after rewarming if TTM used)
Acute Atrial Fibrillation
NICE NG196 · Rate vs rhythm · CHA₂DS₂-VASc · Anticoagulation
NICE NG196Haemodynamic instability? SBP <90, severe LVF, ongoing ischaemia, syncope → Immediate synchronised DC cardioversion. Call senior/cardiology.
- 112-lead ECG: confirm AF. Exclude WPW (broad complex irregular → avoid AV nodal blockers).
- 2Bloods: FBC, U&E, TFTs, CRP, troponin, coagulation, LFTs, Mg²⁺
- 3Onset timing: <48h vs ≥48h — critical for cardioversion strategy
- 4Haemodynamics: HR, BP, SpO₂, conscious level, signs of LVF
- 5CXR: pulmonary oedema, infection, cardiomegaly
- 6Identify triggers: sepsis, thyrotoxicosis, PE, electrolyte disturbance, ACS, alcohol
Target HR: <110 bpm (RACE II). Tighter <80 bpm if symptomatic or reduced EF.
Do NOT combine beta-blocker + diltiazem/verapamil → risk of complete heart block.
AF <48h onset
Cardioversion can proceed without TOE. Start anticoagulation before/at time. Continue ≥4 weeks post-cardioversion.
AF ≥48h or unknown onset
Must be anticoagulated ≥3 weeks before cardioversion, OR perform TOE to exclude LA thrombus. Continue ≥4 weeks post.
| Risk Factor | Score |
|---|---|
| Congestive heart failure / LV dysfunction | 1 |
| Hypertension | 1 |
| Age ≥75 years | 2 |
| Diabetes mellitus | 1 |
| Stroke / TIA / TE history | 2 |
| Vascular disease (prior MI, PAD, aortic plaque) | 1 |
| Age 65–74 years | 1 |
| Sex: Female | 1 |
Men: anticoagulate if ≥1 | Women: anticoagulate if ≥2
STEMI & NSTEMI
NICE NG185 · Reperfusion · Antiplatelets · Risk stratification · Secondary prevention
NICE NG185STEMI: Door-to-balloon <60 min (primary PCI) or door-to-needle <30 min (thrombolysis). Activate cath lab immediately on ECG diagnosis.
- 112-lead ECG within 10 min of arrival. Repeat if non-diagnostic. Posterior leads if inferior STEMI.
- 2IV access ×2. O₂ only if SpO₂ <94% (hyperoxia is harmful in ACS). Continuous monitoring.
- 3Bloods: troponin, FBC, U&E, coagulation, glucose, lipids, group & save
- 4Antiplatelets immediately (loading doses — see below)
- 5Analgesia: GTN SL, morphine as needed
- 6Primary PCI within 120 min of first medical contact — preferred strategy
- 7If PCI impossible within 120 min → thrombolysis (within 12h of symptom onset)
| GRACE Score | Risk | In-hospital Mortality | Strategy |
|---|---|---|---|
| <109 | Low | <1% | Medical Rx; outpatient angio within 72h |
| 109–140 | Intermediate | 1–3% | Angiography within 72 hours |
| >140 | High | >3% | Angiography within 24 hours |
Immediate angio (<2h): Haemodynamic instability, refractory angina, acute HF, life-threatening arrhythmia, ongoing ST changes.
- Aspirin 75 mg OD indefinitely
- P2Y12 inhibitor (ticagrelor 90 mg BD or clopidogrel 75 mg OD) × 12 months
- Beta-blocker: Bisoprolol 2.5–10 mg OD (all post-MI)
- ACE inhibitor: Ramipril 2.5 mg OD → titrate to 10 mg OD (especially if EF <40%)
- Statin: Atorvastatin 80 mg OD (high-intensity)
- Eplerenone 25–50 mg OD if EF ≤40% + HF/diabetes (start in hospital)
Supraventricular Tachycardia (SVT)
NICE NG241 · Vagal → Adenosine → Verapamil → DC cardioversion
NICE NG241Haemodynamic instability? SBP <90, AMS, severe chest pain → Synchronised DC cardioversion 50–100 J immediately (sedate first).
Acute Heart Failure
NICE NG106 · Acute pulmonary oedema · Cardiogenic shock · Inotropes
NICE NG106Cardiogenic shock (SBP <90, cold peripheries, oliguria, confusion) → ITU/Cardiology urgently. Consider IABP or percutaneous mechanical support.
- 1Sit upright. High-flow O₂ if SpO₂ <94%. Continuous cardiac monitoring.
- 212-lead ECG: acute MI, AF, arrhythmia as precipitant
- 3Bloods: BNP/NT-proBNP, troponin, FBC, U&E, ABG, LFTs, TFTs, glucose
- 4CXR: bat-wing oedema, cardiomegaly, pleural effusions, Kerley B lines
- 5Bedside echo (POCUS): EF, wall motion, pericardial effusion, IVC
- 6IV access × 2. Urinary catheter — hourly UO monitoring.
BNP >400 ng/L or NT-proBNP >2000 ng/L supports AHF. Values <100/300 ng/L make HF unlikely.
Hyperkalaemia
K⁺ >5.5 mmol/L · ECG-guided emergency management · NICE / UK Renal Association
UK Renal Assoc 2020Mild (5.5–5.9)
Often asymptomatic. Peaked T waves. Treat cause. Dietary K⁺ restriction. Repeat K⁺ in 2–4h.
Moderate (6.0–6.4)
Peaked T waves. Consider nebulised salbutamol + Lokelma/Resonium. Continuous monitoring.
Severe (6.5–6.9)
PR prolongation, wide QRS, loss of P waves. Full treatment protocol. Nephrology if AKI.
Life-threatening (≥7.0)
Sinusoidal/sine wave, VF risk. Calcium immediately + all measures. ICU. Emergency RRT.
Any ECG changes with K⁺ ≥6.0 → Calcium gluconate IV immediately — do not wait for further results.
Progressive ECG sequence: Peaked T waves → Short QT → PR prolongation → Wide QRS → Loss of P waves → Sine wave → VF / Asystole
- Stop ACE inhibitors, ARBs, NSAIDs, K⁺-sparing diuretics, trimethoprim
- Treat AKI: fluid resuscitation, catheter, nephrology review
- Treat DKA: insulin shifts K⁺ into cells (monitor closely)
- Correct acidosis if severe
Acute Asthma Attack
BTS/SIGN 2019 · NICE NG80 · Severity stratification & stepwise management
BTS/SIGN · NICE NG80Moderate
PEFR 50–75% best
No severe features
Increasing symptoms
SpO₂ ≥92%
Severe
PEFR 33–50% best
RR ≥25/min
HR ≥110/min
Cannot complete sentences
SpO₂ <92%
Life-threatening
PEFR <33% best
SpO₂ <92%
PaO₂ <8 kPa
Normal PaCO₂ (4.6–6 kPa)
Silent chest · Cyanosis
Feeble resp effort
Bradycardia · Hypotension
Exhaustion · Confusion
Near-fatal
Raised PaCO₂ >6 kPa
Requiring mechanical ventilation with raised inflation pressures
Life-threatening / near-fatal: Silent chest, cyanosis, feeble respirations, bradycardia, exhaustion, reduced GCS → Senior/ITU immediately
- 1High-flow O₂ 15 L/min via NRB mask — target SpO₂ 94–98%
- 2SABA nebuliser: Salbutamol 5 mg (oxygen-driven). Repeat every 15–20 min. Back-to-back if life-threatening.
- 3Ipratropium 500 mcg neb (add to salbutamol in severe/life-threatening) q4–6h
- 4Systemic steroid immediately — oral preferred
- 5IV access. Bloods: ABG, FBC, U&E, CRP. Cultures if infection suspected.
- 6If life-threatening & poor response: add Mg sulphate IV. Alert anaesthetics/ITU.
- Life-threatening / near-fatal
- Persistent severe features after 1h
- PEFR <75% after treatment
- Nocturnal presentation
- Previous near-fatal episode
- PEFR ≥75%, SpO₂ ≥94% on air
- Symptoms resolved
- Prednisolone prescribed × 5 days
- Inhaler technique checked
- GP follow-up arranged <48h
Acute COPD Exacerbation
NICE NG115 · Controlled O₂ · Bronchodilators · NIV indications
NICE NG115Target SpO₂: 88–92% in COPD. Use 24% or 28% Venturi mask. Avoid hyperoxia — worsens hypercapnia. ABG immediately.
- 1ABG immediately (pH, PaCO₂, PaO₂, HCO₃⁻, BE) — essential for NIV decision
- 2FBC, U&E, CRP, sputum culture, blood cultures if febrile; theophylline level if applicable
- 3CXR: consolidation, pneumothorax, pulmonary oedema
- 4ECG: cor pulmonale arrhythmia, RV strain pattern
| Parameter | Mild | Moderate | Severe |
|---|---|---|---|
| SpO₂ | ≥94% | 88–94% | <88% |
| RR | <20 | 20–24 | ≥25 |
| pH | ≥7.35 | 7.30–7.35 | <7.30 |
| Consciousness | Alert | Alert/confused | Confused/obtunded |
Start NIV early in acute hypercapnic respiratory failure with acidosis — do not delay. NIV reduces mortality and intubation rates in COPD (NICE NG115).
- Facial trauma/burns precluding mask
- Respiratory arrest / gasping
- Fixed upper airway obstruction
- Undrained pneumothorax
- GCS <8 / unable to protect airway
- Recent upper GI or oesophageal surgery
- Bowel obstruction / active vomiting
- pH <7.15 (consider direct intubation)
- Severe haemodynamic instability
- Copious secretions/inability to clear
- Agitation/non-cooperative patient
- Multiorgan failure
pH <7.25 after 1h of NIV, or initial pH <7.15 → ITU/senior immediately. May need intubation & mechanical ventilation.
DKA & HHS
JBDS 2023 · FRII · Fluid resuscitation schedule · Potassium replacement · HHS protocol
JBDS 2023DKA Diagnostic Triad: Blood glucose >11 mmol/L (or known T1DM), Blood/urine ketones ≥3.0 mmol/L (or urine ≥2+), pH <7.3 OR HCO₃⁻ <15 mmol/L
Mild DKA
pH 7.25–7.30
HCO₃⁻ 15–18
Ketones ≥3 mmol/L
Alert
Moderate DKA
pH 7.00–7.24
HCO₃⁻ 10–14
Alert or drowsy
Severe DKA
pH <7.00
HCO₃⁻ <10
GCS <12
K⁺ <3.5
SpO₂ <92%
→ HDU/ITU
- Blood ketones <0.6 mmol/L AND pH >7.3 AND HCO₃⁻ >18 AND patient eating/drinking
- Give SC insulin 30–60 min BEFORE stopping FRII
- Never stop FRII without starting SC insulin first — risk of rebound ketoacidosis
HHS criteria: Glucose >30 mmol/L · Osmolality >320 mOsm/kg · Minimal/no ketones (<3 mmol/L) · No significant acidosis (pH >7.3) · Usually T2DM · Older patients · Higher mortality than DKA
Paracetamol Overdose
MHRA 2012 / NICE CG89 · Rumack-Matthew nomogram · NAC protocol · Hepatic failure
MHRA 2012 · NICE CG89Paracetamol OD is the most common cause of acute liver failure in the UK. Time to treatment is critical — NAC is highly effective if given early. Always contact NPIS (0344 892 0111) for staggered/unknown doses.
- 1Time of ingestion: single acute vs staggered (multiple doses over >1h) vs unknown — staggered/unknown → treat with NAC without waiting for nomogram
- 2Dose taken (mg, tablet count), any co-ingestions (opioids — delays absorption)
- 3Bloods: paracetamol level (≥4h post-ingestion), LFTs, INR/PT, U&E, FBC, glucose, VBG/ABG, lactate
- 4ECG, toxicology screen if co-ingestion suspected
- 5Risk factors for hepatotoxicity: enzyme-inducing drugs (carbamazepine, rifampicin, phenytoin, St John's Wort), chronic alcohol excess, malnutrition, eating disorders, HIV
UK uses a SINGLE treatment line since 2012 MHRA update — no separate "high-risk" line. All patients plot above this line require NAC.
Do NOT use nomogram for: Staggered overdose · Ingestion time unknown · Presentation >24h · Co-ingestion of enzyme inducers (controversial — NPIS guidance). In all these cases: start NAC immediately without waiting.
NAC is most effective within 8h of ingestion. Efficacy decreases but still beneficial up to 24h and beyond in severe toxicity. Do not withhold if late presentation with elevated LFTs/INR.
NAC anaphylactoid reactions: Occur in ~5–15%, usually during Bag 1 (flushing, urticaria, bronchospasm, hypotension). Stop infusion. Give Chlorphenamine 10 mg IV + Salbutamol neb if bronchospasm. Restart at lower rate after 1h. Rarely need to stop permanently.
- Repeat: LFTs, INR/PT, U&E, creatinine, glucose, VBG
- Discharge criteria: LFTs normal or improving, INR <1.3, asymptomatic, no encephalopathy, creatinine normal
- Continue NAC (extend Bag 3 at same rate) if: LFTs rising, INR >1.3 or rising, encephalopathy, renal impairment
Refer urgently to liver transplant centre if ANY of:
- IV glucose (10% dextrose) — monitor closely, hypoglycaemia is life-threatening
- Vitamin K 10 mg IV OD (if coagulopathy)
- FFP only if active bleeding or invasive procedure (do NOT give to normalise INR alone — masks progression)
- Phosphate replacement if hypophosphataemia (refeeding syndrome-like)
- Lactulose 30–50 mL TDS if encephalopathy
- HDU/ICU: ICP monitoring if grade III/IV encephalopathy; avoid sedation
- Contact NPIS (0344 892 0111) and liver transplant centre early
Acute Stroke & TIA
NICE NG128 · Alteplase · Thrombectomy · TIA risk stratification
NICE NG128TIME IS BRAIN — 1.9 million neurons die per minute. Door-to-CT <25 min. Thrombolysis decision <60 min of arrival.
- 1FAST assessment. Activate stroke team immediately. NIL by mouth until swallow assessment.
- 2Non-contrast CT head within 25 min (exclude haemorrhage before any treatment)
- 3CT angiography (CTA) if eligible for thrombectomy
- 4Bloods: glucose, FBC, coag, troponin. 12-lead ECG.
- 5Blood glucose: treat if <4 or >11 mmol/L
- 6Temperature: treat fever >37.5°C with paracetamol 1 g PO/IV QDS
- 7O₂ only if SpO₂ <94%. Avoid routine O₂ in normoxic patients.
- 8BP: see management below
- NO antiplatelets, anticoagulants, or thrombolytics
- Reverse anticoagulation urgently: PCC 25–50 units/kg IV (warfarin); Idarucizumab (dabigatran); Andexanet alfa (apixaban/rivaroxaban)
- BP target: SBP <140 mmHg within 6h (if SBP 150–220 and no contraindication)
- Neurosurgical review: cerebellar haemorrhage >3 cm or obstructive hydrocephalus
| Feature | Score |
|---|---|
| Age ≥60 years | 1 |
| Blood pressure ≥140/90 at presentation | 1 |
| Clinical: unilateral weakness | 2 |
| Clinical: speech impairment without weakness | 1 |
| Duration ≥60 min | 2 |
| Duration 10–59 min | 1 |
| Diabetes present | 1 |
ABCD2 0–3 (Low)
TIA clinic within 7 days. Aspirin 300 mg immediately.
ABCD2 ≥4 (High)
Same-day specialist assessment. Aspirin 300 mg now. Urgent brain + vascular imaging.
Crescendo TIA (≥2 TIAs in 1 week) → admit to acute stroke unit immediately. Risk of stroke in 48h is up to 10%.
Status Epilepticus
NICE NG217 · Convulsive status in adults · Time-critical treatment ladder
NICE NG217Status = seizure ≥5 min OR ≥2 seizures without full recovery. Each minute of untreated seizure causes irreversible neuronal damage. Start treatment immediately — do not wait 5 minutes to act.
Avoid in women of childbearing age (teratogenic), liver disease, mitochondrial disease
- Blood glucose: BM — if <4 mmol/L → Dextrose 100 mL 20% IV (or 50 mL 50%)
- Thiamine 200 mg IV (Pabrinex) BEFORE glucose if alcohol excess/malnutrition — prevents Wernicke's
- ABG, U&E (Na⁺, Ca²⁺, Mg²⁺), FBC, LFTs, AED levels, toxicology screen, CRP, cultures
- CT head when stabilised (structural cause, haemorrhage)
- LP after CT if meningitis/encephalitis suspected
- Treat Na⁺ <125 mmol/L, Ca²⁺ <2.0 mmol/L, Mg²⁺ <0.7 mmol/L
- Antibiotics + Aciclovir if encephalitis possible (see Sepsis section)
Acute PE & DVT
NICE NG158 · Wells score · sPESI · Anticoagulation · Massive PE · Duration
NICE NG158Massive PE (High-risk): SBP <90 mmHg or haemodynamic collapse → Emergency management. Do not wait for imaging if arrest imminent.
| Feature | Score |
|---|---|
| Clinical signs of DVT | 3 |
| PE most likely diagnosis | 3 |
| HR >100 bpm | 1.5 |
| Immobilisation ≥3d / surgery <4wk | 1.5 |
| Prior DVT/PE | 1.5 |
| Haemoptysis | 1 |
| Malignancy | 1 |
>4: PE likely → CT-PA | ≤4: D-dimer; if ↑ → CT-PA
| Factor | Score |
|---|---|
| Age >80 | 1 |
| Cancer | 1 |
| Chronic cardiopulmonary disease | 1 |
| HR ≥110 bpm | 1 |
| SBP <100 mmHg | 1 |
| SpO₂ <90% | 1 |
sPESI 0 Low risk — consider early discharge | sPESI ≥1 Admit
Start therapeutic anticoagulation immediately on clinical suspicion of PE/DVT (before imaging if high clinical probability), unless major bleeding contraindication.
| Scenario | Duration | Notes |
|---|---|---|
| Provoked PE/DVT (major transient: surgery, trauma) | 3 months | Low recurrence risk after stopping |
| Unprovoked PE/DVT (first episode) | ≥3 months; consider extended | Weigh recurrence risk vs bleeding |
| Second unprovoked VTE | Indefinite | Reassess annually |
| Cancer-associated VTE | Active cancer / throughout treatment | LMWH or edoxaban/rivaroxaban |
| Antiphospholipid syndrome | Indefinite | Warfarin (INR 2–3); DOACs controversial |
| Provoked DVT (minor transient) | 3 months | e.g., travel, oestrogen, minor injury |
Massive PE = SBP <90 mmHg >15 min, syncope, shock, or cardiac arrest due to PE. Immediate thrombolysis unless contraindicated. Senior/cardiology/cardiothoracics urgently.
- 1High-flow O₂. IV access ×2. Crash team if arresting.
- 2Bedside echo: RV dilation, D-sign, McConnell's sign
- 3CT-PA if patient stable enough — do NOT delay treatment if very unstable
- 4UFH 80 units/kg IV bolus immediately
- 5Systemic thrombolysis if no contraindication (see Thrombolysis section)
- 6If thrombolysis CI / failed → surgical embolectomy or catheter-directed thrombolysis
- 7Noradrenaline for haemodynamic support
Wells DVT: Score ≥2 → USS | Score <2 → D-dimer; if ↑ → USS. Treat with same anticoagulation as PE. Routine compression stockings NOT recommended for PTS prevention (NICE NG158).
Thrombolysis — Contraindications
STEMI · Acute ischaemic stroke · Massive PE · Drug doses
NICE / SIGN / RCUKIf ANY absolute CI present → DO NOT thrombolyse. For STEMI: proceed to primary PCI. For PE: surgical embolectomy or catheter-directed lysis.
| Contraindication | Applies to |
|---|---|
| Haemorrhagic stroke or stroke of unknown origin (any time) | All |
| Ischaemic stroke in preceding 6 months | STEMI / PE (stroke itself may qualify within 4.5h) |
| CNS neoplasm, AVM, or aneurysm | All |
| Major trauma / surgery / head injury <3 weeks | All |
| Active internal bleeding (not menstruation) | All |
| Suspected aortic dissection | All |
| Non-compressible arterial puncture <24h (lumbar puncture, liver biopsy) | All |
| Active bleeding diathesis | All |
| Platelet count <100,000/mm³ | All |
| BP >185/110 mmHg uncontrolled (for stroke alteplase) | Stroke |
| Current anticoagulation therapeutic levels (INR >1.7, DOAC within 48h) | Stroke |
| Blood glucose <2.7 or >22 mmol/L (confounds diagnosis) | Stroke |
- TIA in preceding 6 months
- Oral anticoagulant use (not within therapeutic range)
- Pregnancy or within 1 week postpartum
- Refractory hypertension (SBP >180 mmHg)
- Advanced liver disease / cirrhosis
- Infective endocarditis
- Active peptic ulcer
- Prolonged or traumatic CPR (>10 min)
Acute Sepsis
NICE NG51 · Sepsis-6 · Antibiotics by source · Vasopressors · ICU criteria
NICE NG51 · Sepsis-3qSOFA (≥2 = screen for sepsis)
Altered mental status
RR ≥22/min
SBP ≤100 mmHg
Septic Shock
Sepsis + vasopressor to maintain MAP ≥65 + lactate >2 mmol/L despite adequate fluid. Mortality >40%.
- Altered mentation (confusion, agitation, reduced GCS)
- RR ≥25/min
- SBP ≤90 mmHg (or >40 mmHg drop from baseline)
- HR ≥130 bpm
- SpO₂ <91% on air
- Not passed urine in 18h (UO <0.5 mL/kg/h)
- Mottled/ashen/cyanotic appearance
- Non-blanching rash (meningococcal septicaemia)
- 1Blood cultures ×2 sets before antibiotics (do not delay abx)
- 2IV antibiotics within 1 hour of recognition (high-risk); 3 hours for moderate-risk
- 3Serum lactate: if >2 mmol/L indicates tissue hypoperfusion
- 4IV fluid resuscitation if hypotensive or lactate >2
- 5High-flow O₂ — target SpO₂ ≥94% (88–92% in COPD)
- 6Urine output monitoring — catheterise; target UO >0.5 mL/kg/h
Always follow local antimicrobial guidelines. De-escalate within 48–72h based on cultures. These are starting-point empiric regimens per NICE NG51 / PHE.
| Source | First-line | Penicillin Allergy |
|---|---|---|
| Unknown / NOS | Pip-tazo 4.5 g IV TDS | Meropenem 1 g IV TDS or Vancomycin + Gentamicin |
| CAP (severe) | Co-amoxiclav 1.2 g IV TDS + Clarithromycin 500 mg IV BD | Levofloxacin 500 mg IV BD + Clarithromycin |
| HAP / VAP | Pip-tazo 4.5 g IV TDS ± Gentamicin | Meropenem 1 g IV TDS ± Vancomycin |
| Urosepsis | Co-amoxiclav 1.2 g IV TDS (or Cefuroxime 1.5 g IV TDS) | Gentamicin 5 mg/kg OD IV |
| Intra-abdominal | Pip-tazo 4.5 g IV TDS | Meropenem 1 g IV TDS + Metro 500 mg IV TDS |
| Meningitis | Ceftriaxone 2 g IV BD + Dexamethasone 0.15 mg/kg IV QDS × 4d | Chloramphenicol 25 mg/kg IV QDS |
| Encephalitis (HSV) | Aciclovir 10 mg/kg IV TDS × 14–21 days | Same |
| Skin / necrotising | Pip-tazo 4.5 g IV TDS + Clindamycin 1.2 g IV TDS | Meropenem + Clindamycin + Vancomycin |
| Neutropenic sepsis | Pip-tazo 4.5 g IV TDS (per local policy) | Meropenem 1 g IV TDS |
- Vasopressor requirement to maintain MAP ≥65 mmHg
- Lactate ≥4 mmol/L despite resuscitation
- Need for mechanical ventilation (GCS ≤8, RR >35, SpO₂ <88% on 60% O₂)
- AKI requiring RRT
- Multiorgan dysfunction (≥2 systems)
Anaphylaxis
NICE NG212 · RCUK 2021 · Adrenaline IM is ALWAYS first-line
NICE NG212 · RCUK 2021Anaphylaxis = sudden life-threatening airway ± breathing ± circulation problems, usually with skin/mucosal changes. Adrenaline IM is ALWAYS first-line — administer immediately. Never delay it.
- 1Remove trigger. Call for help / crash team. Lie flat + legs raised (unless airway compromise — sit upright).
- 2Adrenaline IM immediately — see dose below. Do not delay for any other treatment.
- 3High-flow O₂ 15 L/min via NRB mask. Prepare to intubate if airway swelling.
- 4IV access ×2. IV fluid bolus if hypotensive.
- 5Continuous monitoring: HR, BP, SpO₂, ECG, 12-lead when stable.
- 6Repeat adrenaline every 5 min if no response (no maximum dose).
- 7Antihistamine + hydrocortisone AFTER adrenaline has been given.
Biphasic reaction: Recurrence 1–72h (typically 8–12h) after initial resolution without re-exposure. Observe all patients minimum 6–12 hours.
- Severe reaction (respiratory arrest / circulatory collapse)
- Required >1 dose adrenaline
- Co-morbid asthma (especially poorly controlled)
- Evening/night presentation (reduced community support)
- Idiopathic anaphylaxis (no identifiable trigger)
- Discharge with 2 adrenaline auto-injectors — prescribe and demonstrate technique
- Written anaphylaxis action plan
- Prednisolone 50 mg OD × 3 days + Cetirizine 10 mg OD × 3 days
- Referral to allergy specialist clinic within 1–2 months
- Medical alert bracelet advised
Massive Haemorrhage
NICE NG39 · MHP activation · 1:1:1 transfusion ratio · TXA · Anticoagulant reversal
NICE NG39Activate Massive Haemorrhage Protocol (MHP). Call senior, haematologist, blood bank. Permissive hypotension: target SBP 80–90 mmHg until surgical haemostasis — EXCEPT TBI (target SBP ≥100 mmHg).
- 1Direct pressure / tourniquets / wound packing for external bleeding — FIRST priority.
- 2IV access ×2 large-bore (14G). IO access if IV impossible (sternal IO for better flow).
- 3Group & save + crossmatch. FBC, clotting, fibrinogen, TEG/ROTEM if available, ABG, lactate, Ca²⁺.
- 4Activate MHP → O-negative blood immediately if exsanguinating (do NOT wait for crossmatch).
- 5Transfuse in 1:1:1 ratio (pRBC : FFP : Platelets).
- 6Tranexamic acid (TXA) immediately if within 3 hours of injury onset.
- 7Warm all blood products (use fluid warmer / level 1). Target core temperature >36°C.
- 8Surgical / IR haemostasis — do not delay. This is the definitive treatment.
| Anticoagulant | Reversal Agent | Dose | Onset |
|---|---|---|---|
| Warfarin | 4-factor PCC (Beriplex/Octaplex) + Vit K | PCC 25–50 units/kg IV (INR-based) + Vit K 10 mg IV slow | Minutes |
| Dabigatran | Idarucizumab (Praxbind) | 5 g IV (2 × 2.5 g vials) | <5 min |
| Apixaban / Rivaroxaban | Andexanet alfa (Ondexxya) | 400–800 mg IV bolus then infusion (specialist) | Minutes |
| Apixaban / Rivaroxaban (no Andexanet) | 4-factor PCC (unlicensed) | 50 units/kg IV — haematology guidance | Minutes |
| UFH | Protamine sulphate | 1 mg per 100 units UFH in last 4h (max 50 mg IV slow) | 5 min |
| LMWH (e.g., enoxaparin) | Protamine sulphate (partial ~60%) | 1 mg per 1 mg (100 units) enoxaparin; max 50 mg IV | 5 min |
| Fondaparinux | rFVIIa (unlicensed) | Haematology guidance — no licensed specific antidote | Variable |
Protamine sulphate can cause severe allergic reactions (more common in fish allergy / prior protamine exposure). Have resuscitation equipment available.
Hypothermia
Target >36°C. Warm IV fluids, active external warming blankets, warm blood products. Hypothermia impairs coagulation cascade.
Acidosis
Target pH >7.2. Correct with adequate resuscitation and haemostasis. Bicarbonate only if pH <7.1 and not responding.
Coagulopathy
1:1:1 ratio. Fibrinogen >2 g/L. TEG/ROTEM-guided if available. Avoid excessive crystalloid (dilutes clotting factors).
Hypertension & Hypertensive Crisis
NICE NG136 (updated 2023) · Hypertensive emergency vs urgency · Target organ damage
NICE NG136Hypertensive emergency = BP ≥180/120 mmHg + acute target organ damage (encephalopathy, AKI, pulmonary oedema, aortic dissection, eclampsia, retinal haemorrhage). Requires IV treatment in monitored setting.
Stage 1 Hypertension
Clinic ≥140/90 & ABPM ≥135/85 mmHg. Treat if age <80 + ≥10% 10yr CVD risk, TOD, diabetes, CKD, or CVD.
Stage 2 Hypertension
Clinic ≥160/100 or ABPM ≥150/95 mmHg. Offer antihypertensive drug treatment regardless of CVD risk.
Severe Hypertension
Clinic SBP ≥180 or DBP ≥120 mmHg. Assess for TOD — if absent: urgency management, not emergency.
Hypertensive Emergency
Any BP + acute TOD. Encephalopathy, eclampsia, aortic dissection, acute pulmonary oedema, AKI, papilloedema, retinal haemorrhages.
NICE NG136: Hypertensive urgency (severe BP without TOD) — do NOT lower BP too rapidly. Restart/optimise oral agents. Aim BP ≤160/100 within 24–48h. IV agents usually NOT required.
- 1ICU/HDU admission. Continuous arterial line monitoring. IV access.
- 2Investigations: ECG, FBC, U&E, creatinine, urine dip, LFTs, troponin, CXR, CT head, fundoscopy.
- 3Target: reduce MAP by no more than 20–25% in first hour, then to ~160/100 over next 2–6h.
- 4Exception — aortic dissection: target SBP <120 mmHg within 20 min (with labetalol ± SNP).
- 5Exception — eclampsia/pre-eclampsia: target SBP 130–150 mmHg. Labetalol or hydralazine.
- 6Haemorrhagic stroke: reduce SBP to <140 mmHg within 1h if SBP >220 mmHg (per NICE).
- 7Avoid precipitous drops — can cause cerebral/coronary ischaemia.
| Step | Age <55 / Non-Black | Age ≥55 or Black African/Caribbean |
|---|---|---|
| Step 1 | ACE inhibitor or ARB Ramipril 2.5→10 mg OD / Losartan 50→100 mg OD | CCB Amlodipine 5→10 mg OD |
| Step 2 | ACE inhibitor/ARB + CCB Combine step 1 agents | |
| Step 3 | ACE inhibitor/ARB + CCB + Thiazide-like diuretic Indapamide 1.5 mg MR OD or Chlortalidone 25 mg OD | |
| Step 4 | Review adherence. Add: Spironolactone 25 mg OD (if K⁺ ≤4.5), beta-blocker, or alpha-blocker. Refer specialist. | |
BP targets (NICE NG136): Age <80: clinic <140/90 (ABPM <135/85). Age ≥80: clinic <150/90. Diabetics: <140/90. CKD with albuminuria: <130/80.
Diabetes Management
NICE NG28 (T1DM) · NG87 (T2DM) · NG17 (Inpatient) · Hypoglycaemia · SGLT2i · GLP-1
NICE NG28 / NG87Hypoglycaemia emergency: BG <4.0 mmol/L with symptoms or BG <3.0 mmol/L — treat immediately. If unconscious: IV glucose or glucagon.
Conscious & able to swallow
15–20 g fast-acting carbohydrate (150–200 mL fruit juice, 5 glucose tablets, or Glucogel). Repeat after 15 min if BG still <4.
Unconscious / unable to swallow
IV glucose or IM glucagon. Do NOT give oral glucose — aspiration risk.
Sulphonylurea-induced hypoglycaemia: risk of prolonged recurrent episodes. Admit for monitoring ≥24h. Consider octreotide 50 mcg SC TDS in severe cases.
| Patient Group | HbA1c Target |
|---|---|
| Managed with lifestyle/metformin only | 48 mmol/mol (6.5%) |
| On drug with hypoglycaemia risk (SU, insulin) | 53 mmol/mol (7.0%) |
| Age ≥65, frail, or multiple comorbidities | Individualise — avoid hypoglycaemia |
| Type 1 diabetes | 48 mmol/mol (6.5%) with flash/CGM-assisted care |
NICE NG28: Offer flash glucose monitoring (FreeStyle Libre) or CGM to all adults with T1DM. Offer insulin pump therapy if multiple injections fail to achieve HbA1c <69 mmol/mol.
- Target BG 6–10 mmol/L (acceptable 4–12) during admission
- Variable Rate Insulin Infusion (VRIII/sliding scale) only if patient is NBM >1 meal, vomiting, or perioperative
- Continue usual subcutaneous insulin where possible — review doses
- Stop metformin if eGFR <30, contrast media, or sepsis
- Stop SGLT2i at admission (DKA risk). Restart 48–72h after recovery.
- BG monitoring: 4–6 hourly on insulin; pre-meal and bedtime if diet-controlled
- Diabetes specialist nurse review within 24h if available
Malignant Spinal Cord Compression
NICE NG234 (2023) · Emergency · Dexamethasone · Whole-spine MRI · Neurosurgery within 24h
NICE NG234 · 2023MSCC is an oncological emergency. Any cancer patient with new back pain + neurology (weakness, sensory level, bladder/bowel dysfunction) → immediate whole-spine MRI within 24h. Do NOT wait for imaging before starting dexamethasone if neurology present.
- Back pain in known cancer patient (especially progressive, worse lying flat/at night)
- New limb weakness, paraesthesia, or sensory level
- Bladder or bowel dysfunction (retention, incontinence)
- Difficulty walking or gait ataxia
- New radicular pain below neck in cancer patient
Over 20% of patients with MSCC have NO prior cancer diagnosis. Consider MSCC in any patient with these features even without known malignancy.
- 1Full neurological exam: motor, sensory level, reflexes, anal tone, PR if appropriate.
- 2Contact MSCC coordinator / oncology immediately on clinical suspicion.
- 3Whole-spine MRI (gold standard) — request urgently. If MRI contraindicated: whole-spine CT with contrast.
- 4If spinal instability suspected: do not mobilise until imaging/surgical opinion obtained.
Dexamethasone side effects: hyperglycaemia (check BG 6-hourly), GI bleeds (give PPI), psychosis, fluid retention. Prescribe PPI prophylaxis (Omeprazole 20 mg OD) with dexamethasone.
| Scenario | Treatment | Timing |
|---|---|---|
| MSCC suitable for surgery + good prognosis | Surgical decompression ± stabilisation | Within 24h of diagnosis |
| MSCC not suitable for surgery | Urgent radiotherapy | As soon as possible, within 24h |
| Complete paralysis ≥48h, pain controlled | Palliative radiotherapy or best supportive care | Senior/palliative decision |
| Haematological malignancy (lymphoma) | Radiotherapy ± chemotherapy — haematology MDT | Urgent |
- Physiotherapy and occupational therapy from day 1
- Bladder management: catheterisation if retention, ISC if able
- Bowel regimen: laxatives, suppositories
- Thromboprophylaxis (VTE): LMWH — discuss with neurosurgery post-op
- Pressure area care: 2-hourly turns, pressure mattress
- Rehab team referral, palliative care MDT input
Subarachnoid Haemorrhage (SAH)
AHA/ASA 2023 Guideline · NICE guidance · Thunderclap headache · CT + LP · Nimodipine · Neurosurgery
AHA/ASA 2023 · NICE"Worst headache of my life" / thunderclap headache = SAH until proven otherwise. CT head immediately. If CT negative and <6h: CT negative does NOT exclude SAH — LP required (or CTA as per local protocol).
- Sudden-onset severe headache ("thunderclap") — maximal at onset within seconds
- Neck stiffness (meningism) — may take hours to develop
- Photophobia, nausea, vomiting
- Brief loss of consciousness at onset
- Focal neurology, cranial nerve palsy (CN III — posterior communicating artery aneurysm)
- Sentinel headache in preceding weeks (suggests warning leak)
| WFNS Grade | GCS | Motor Deficit | Prognosis |
|---|---|---|---|
| Grade I | 15 | None | Good |
| Grade II | 13–14 | None | Good |
| Grade III | 13–14 | Present | Moderate |
| Grade IV | 7–12 | ± | Poor |
| Grade V | 3–6 | ± | Very poor |
- 1Bed rest. Quiet environment. Continuous monitoring. IV access ×2.
- 2Analgesia: paracetamol ± opioid (see below). Avoid NSAIDs (platelet inhibition).
- 3Antiemetics: ondansetron 4 mg IV or metoclopramide 10 mg IV.
- 4Start Nimodipine immediately for vasospasm prevention.
- 5BP management: avoid SBP >160 mmHg prior to aneurysm treatment. Labetalol if needed.
- 6Neurosurgical referral urgently — aim for aneurysm treatment within 24–48h.
- 7Maintain euvolaemia — isotonic fluids. Avoid hypervolaemia.
- 8ECG (SAH causes Wellens-like ECG changes, prolonged QT, T-wave inversions).
- 9U&E, FBC, coagulation, glucose. Correct hyponatraemia (risk of hyponatraemic vasospasm).
Re-bleeding
Highest risk first 24h. Maintain controlled BP. Urgent aneurysm treatment (clipping or coiling) within 24h.
Vasospasm / DCI
Days 4–14. TCD monitoring. Nimodipine. HHH therapy (hypertension, hypervolaemia, haemodilution — now selective). IA vasodilators if severe.
Hydrocephalus
Early or late. CT scan if deterioration. External ventricular drain (EVD) if symptomatic acute hydrocephalus.
Hyponatraemia
SIADH or cerebral salt wasting. SIADH: fluid restrict. Cerebral salt wasting: fluid + salt replacement. Avoid rapid correction.
Neuropathic Pain
NICE CG173 (updated 2023) · Amitriptyline · Duloxetine · Gabapentin · Pregabalin
NICE CG173- Burning, shooting, stabbing, electric-shock like quality
- Allodynia (pain from non-painful stimulus) or hyperalgesia
- Spontaneous pain — constant or paroxysmal
- Sensory deficit in area of pain
- Common causes: diabetic neuropathy, post-herpetic neuralgia, trigeminal neuralgia, post-surgical/traumatic, chemotherapy-induced, central post-stroke pain, phantom limb, radiculopathy
Use validated tools: DN4 or painDETECT for screening. Assess severity (NRS 0–10), sleep, mood, function, and quality of life at each review.
Paracetamol and NSAIDs are NOT recommended as first-line for neuropathic pain (NICE CG173). They have limited efficacy for nerve pain.
- Physiotherapy and graded exercise for radiculopathy and central sensitisation
- TENS (transcutaneous electrical nerve stimulation) — some benefit in localised neuropathy
- Psychological support: CBT for pain management — especially if mood/sleep affected
- Refer to specialist pain service if: diagnosis uncertain, inadequate response to 2+ agents, complex psychosocial factors, or complex conditions (e.g., CRPS)
WHO Pain Ladder & Analgesia
WHO 3-Step Ladder · Opioid initiation · Adjuvants · Opioid rotation · NICE guidance
WHO Ladder · BNF · NICE NG31Step 1 — Mild Pain (NRS 1–3)
Non-opioid analgesia:
Paracetamol 1 g QDS ± NSAIDs (Ibuprofen 400 mg TDS, Naproxen 500 mg BD). ± Adjuvants.
Step 2 — Moderate Pain (NRS 4–6)
Weak opioid + non-opioid:
Codeine 30–60 mg q4h ± paracetamol. Or Tramadol 50–100 mg QDS. ± Adjuvants.
Step 3 — Severe Pain (NRS 7–10)
Strong opioid + non-opioid:
Morphine, oxycodone, fentanyl. Titrate to pain. Continue non-opioids. ± Adjuvants.
Principle: "By the clock" (regular dosing), "By mouth" (oral preferred), "By the ladder" (step up), "For the individual" (personalised). Reassess frequently.
| Adjuvant | Indication | Dose |
|---|---|---|
| Amitriptyline | Neuropathic pain | 10–75 mg nocte |
| Gabapentin | Neuropathic, bone pain | 300 mg OD → TDS (max 3600 mg/day) |
| Pregabalin | Neuropathic pain | 75 mg BD → 300 mg BD |
| Dexamethasone | Nerve compression, bone pain, visceral, raised ICP | 4–16 mg PO/IV OD (morning) |
| NSAIDs | Bone pain, inflammation | Ibuprofen 400 mg TDS + PPI (eGFR >30) |
| Bisphosphonates | Bone metastases pain | Zoledronic acid 4 mg IV q4 weeks (specialist) |
| Ketamine | Refractory neuropathic/cancer pain | Specialist use. SC infusion 0.1–0.5 mg/kg/h |
| Lidocaine | Refractory neuropathic pain (ED setting) | 1.5 mg/kg IV over 10 min (specialist) |
| Side Effect | Management |
|---|---|
| Constipation (universal) | Laxatives from day 1: Senna 2–4 tabs BD + Macrogol OD (do not use bulk-forming laxatives) |
| Nausea/vomiting | Metoclopramide 10 mg TDS, Haloperidol 0.5–1.5 mg nocte, Cyclizine 50 mg TDS |
| Sedation | Review dose, exclude other causes. If persistent: consider opioid rotation. |
| Respiratory depression | Naloxone 100–200 mcg IV; repeat every 2 min; infusion 60% of effective dose/h |
| Pruritus | Antihistamine or low-dose naloxone infusion |
| Urinary retention | Catheter, opioid dose reduction, opioid rotation |
| Opioid-induced hyperalgesia | Reduce opioid dose, rotate opioid, add ketamine or alpha-2 agonist |
Palliative Care — Symptom Control
NICE NG31 · End-of-life · Syringe driver · Anticipatory prescribing · Last days of life
NICE NG31- Profound weakness — bedbound, unable to lift arms
- Drowsy/unconscious most of the time, minimal interaction
- Only able to take sips of fluid; difficulty swallowing medications
- Mottled, peripherally cyanosed skin; cool extremities
- Cheyne-Stokes breathing / periods of apnoea
- Oliguria / anuria — dark concentrated urine
When dying is recognised: discuss with patient (if able) and family. Stop inappropriate monitoring/investigations. Ensure anticipatory medications prescribed. Document DNACPR decision. Refer to specialist palliative care if symptoms complex.
Prescribe anticipatory SC medications for: pain, breathlessness, agitation/distress, nausea/vomiting, and respiratory secretions. These should be available at home or bedside for PRN use.
Use a syringe driver (continuous subcutaneous infusion, CSCI) over 24h when oral route is no longer possible. Combine medications cautiously — check compatibility before mixing.
| Oral Drug | SC Equivalent | Ratio |
|---|---|---|
| Morphine PO | Morphine SC | 2:1 (oral 30 mg → SC 15 mg/24h) |
| Oxycodone PO | Oxycodone SC | 2:1 |
| Codeine PO 240 mg | Morphine SC ~12 mg | Codeine:morphine ~20:1 oral then 2:1 |
| Fentanyl patch 25 mcg/h | Morphine SC 30 mg/24h | Approximate |
| Tramadol PO 400 mg | Morphine SC ~20 mg/24h | Approximate |
| Haloperidol PO | Haloperidol SC | 1:1 |
| Midazolam | Midazolam SC | IV dose = SC dose |
Palliative Pain & Malignancy
NICE NG31 · Cancer pain management · Bone metastases · Breakthrough pain · Ketamine
NICE NG31 · ESMO Guidelines- Site and radiation — localised vs referred vs generalised
- Quality — aching (bone), burning/shooting (neuropathic), colicky (visceral), constant (somatic)
- Severity — NRS 0–10 at rest and on movement (incident pain)
- Pattern — continuous background pain vs breakthrough pain vs incident (movement-related)
- Current analgesia and effectiveness — dose, timing, route, side effects
- Functional impact — sleep, mobility, mood, QoL
Background Pain
Continuous, present most of the time. Treat with regular around-the-clock analgesia. Titrate to control.
Breakthrough Pain
Transient flares of pain despite baseline analgesia. Treat with 1/6th of TDD as PRN dose.
Incident Pain
Precipitated by movement or activity (e.g., bone mets). Pre-empt with short-acting opioid 30–45 min before activity.
- 1Assess pain severity (NRS), baseline opioid regimen, last dose and time.
- 2Identify cause: bone fracture, visceral obstruction, infection, MSCC, cord compression — treat underlying cause where possible.
- 3If on regular opioids: give breakthrough dose = 1/6th of TDD SC/IV immediately. Can repeat q20–30 min × 3 if severe.
- 4If opioid-naïve with severe cancer pain: Morphine 2.5–5 mg IV/SC titrated q5–10 min until NRS ≤4.
- 5Add adjuvants: IV dexamethasone 8 mg for nerve compression or bone pain crisis.
- 6Liaise with palliative care team / patient's oncology team. Avoid dose-capping without specialist input.
- 7On discharge: ensure written plan, escalation plan, and palliative care follow-up arranged.
Cancer patients in severe pain should NOT be sent home undertreated. There is no ceiling to opioid dosing in cancer pain — the ceiling is side effects. Involve palliative care early.
Hyponatraemia
Na⁺ <135 mmol/L · NICE CG192 / EASL-ERA Guidelines 2014 · Correction rate critical
EASL-ERA 2014 · NICE CG192Overcorrection risk: Correction >8–10 mmol/L in 24h → Osmotic Demyelination Syndrome (ODS) — irreversible neurological injury. In chronic hyponatraemia: correct at maximum 8 mmol/L per 24h.
Mild (130–135)
Usually asymptomatic. Identify cause. Treat underlying condition. Fluid restrict if SIADH.
Moderate (125–129)
Nausea, confusion, headache. Restrict fluids if SIADH. Seek cause. Monitor 4–6 hourly Na⁺.
Severe (<125)
Vomiting, seizures, coma, cardiorespiratory compromise. EMERGENCY — 3% saline.
| Volume Status | Causes | Management Approach |
|---|---|---|
| Hypovolaemic (dry) | Vomiting, diarrhoea, diuretics, burns, Addison's | IV 0.9% NaCl cautiously |
| Euvolaemic (normal) | SIADH, hypothyroidism, psychogenic polydipsia | Fluid restriction ± vaptans |
| Hypervolaemic (oedematous) | Heart failure, cirrhosis, nephrotic syndrome, AKI/CKD | Fluid restriction + treat cause |
- Plasma osmolality <275 mOsm/kg + Urine osmolality >100 mOsm/kg
- Urine Na⁺ >30 mmol/L (with normal salt intake)
- Clinically euvolaemic
- Normal thyroid, adrenal, renal function; no diuretics
- Common causes: malignancy (lung, CNS), CNS disease, pulmonary disease, drugs (SSRIs, PPIs, carbamazepine, NSAIDs, opioids)
In acute hyponatraemia (<48h duration — e.g., post-operative, marathon runner, MDMA): faster correction to 130 mmol/L is safer as risk of cerebral oedema outweighs ODS risk.
Hypernatraemia
Na⁺ >145 mmol/L · Free water deficit · Diabetes insipidus · Careful correction
BNF · UpToDate 2024Overcorrection of chronic hypernatraemia → cerebral oedema. Maximum correction: 10–12 mmol/L per 24h in chronic (duration >48h). In acute (<24h): can correct to normal faster.
Na 146–150
Mild — usually thirst, irritability. Identify cause. Increase free water intake.
Na 151–159
Moderate — lethargy, weakness, irritability, seizures risk. Active treatment required.
Na ≥160
Severe — confusion, coma, seizures, high mortality. ICU monitoring, careful fluid replacement.
| Cause Category | Examples | Urine Osmolality |
|---|---|---|
| Inadequate water intake | Elderly/disabled, impaired thirst (adipsia) | >600 mOsm/kg (concentrated) |
| Excess water loss | Diarrhoea, fever, burns, insensible loss | >600 mOsm/kg |
| Renal water loss | Diabetes insipidus (central/nephrogenic), osmotic diuresis | <300 mOsm/kg (dilute — DI) |
| Sodium excess | Hypertonic saline, NaHCO₃ overdose, mineralocorticoid excess | Variable |
Hypokalaemia
K⁺ <3.5 mmol/L · ECG changes · IV/PO replacement · NICE / BNF
BNF · UK Renal AssociationHypokalaemia potentiates digoxin toxicity and predisposes to arrhythmias — especially if concurrent hypomagnesaemia. Always correct Mg²⁺ simultaneously.
Mild (3.0–3.5)
Often asymptomatic. Fatigue, muscle cramps. Oral replacement preferred. Dietary increase.
Moderate (2.5–2.9)
Weakness, cramps, constipation, palpitations. ECG changes (U wave). Oral ± IV replacement.
Severe (<2.5)
Profound weakness, paralysis, ventricular arrhythmias (VT/VF risk), rhabdomyolysis. IV replacement urgently.
- Flattening/inversion of T waves
- Prominent U waves (positive deflection after T wave, best seen V2–V3)
- ST depression
- Prolonged QU interval (may look like prolonged QT)
- Wide QRS, ventricular ectopics, VT/VF (severe)
- GI losses: vomiting, diarrhoea, fistulae, ileostomy
- Diuretics (loop, thiazide) — review dose/type
- Hyperaldosteronism, Cushing's syndrome
- Refeeding syndrome
- Magnesium deficiency (refractory hypokalaemia)
- Drugs: insulin, beta-2 agonists, aminoglycosides, amphotericin
Hyperkalaemia — Full Protocol
K⁺ >5.5 mmol/L · UK Renal Association 2020 / NICE · ECG-guided management
UK Renal Assoc 2020 · NICEK⁺ ≥6.5 or any K⁺ with ECG changes (peaked T, wide QRS, sine wave) = EMERGENCY. Start calcium immediately. Call senior.
Mild (5.5–5.9)
Peaked T waves. Treat cause. Dietary restriction. Oral Lokelma/Resonium. Repeat K⁺ 2–4h.
Moderate (6.0–6.4)
Peaked T waves ± prolonged PR. Lokelma. Nebulised salbutamol. Monitor.
Severe (6.5–6.9)
Wide QRS. Calcium + insulin/dextrose + salbutamol. Consider Lokelma. Assess dialysis need.
Life-threatening (≥7.0 or ECG)
Sine wave / VF pattern. Immediate calcium. Full protocol. Dialysis if refractory. Resuscitation team standby.
- 1Calcium gluconate 10% 30 mL IV over 5–10 min (cardiac membrane stabilisation — works within 3 min, lasts 30–60 min). Give first if any ECG changes.
- 2Insulin 10 units Actrapid + 50 mL 50% glucose IV over 15–30 min (lowers K⁺ by 0.6–1 mmol/L within 15–30 min, lasts 4–6h). Monitor BG 30 min, 1h, 2h post.
- 3Salbutamol 10–20 mg nebulised (double/triple dose) — lowers K⁺ by 0.5–1 mmol/L; additive with insulin/dextrose.
- 4Sodium bicarbonate 1.26% 500 mL IV — only if metabolic acidosis (pH <7.2); modest effect alone.
- 5Lokelma (sodium zirconium cyclosilicate) 10 g PO TDS × 48h — fast-acting K⁺ binder; onset 1–2h. Preferred over Resonium. Avoid if ileus.
- 6Stop all potassium-raising drugs: ACEi, ARB, K-sparing diuretics, K supplements, NSAIDs, trimethoprim.
- 7If refractory or AKI/anuria: Emergency haemodialysis — contact renal team urgently.
Hypocalcaemia
Corrected Ca²⁺ <2.1 mmol/L · Tetany · Seizures · IV calcium · Vitamin D
BNF · NICE CKSAcute severe hypocalcaemia (Ca²⁺ <1.8 or symptomatic tetany/seizures/cardiac) → IV calcium gluconate immediately. Secure airway if laryngospasm.
Mild (2.0–2.1)
Often asymptomatic or mild perioral/finger paraesthesia. Oral calcium + vitamin D supplementation.
Moderate (1.8–2.0)
Cramps, Trousseau's sign, Chvostek's sign. ECG: prolonged QT. Oral or IV replacement.
Severe (<1.8)
Tetany, seizures, laryngospasm, bronchospasm, hypotension, arrhythmias. IV calcium urgently.
- Trousseau's sign: inflate BP cuff >systolic for 3 min → carpopedal spasm (more specific)
- Chvostek's sign: tap facial nerve at zygoma → ipsilateral facial twitch (less specific)
- ECG: prolonged QT interval (corrected QTc >440 ms); T-wave changes; risk of Torsades de Pointes
- Corrected calcium = measured Ca²⁺ + 0.02 × (40 − albumin g/L)
- Hypoparathyroidism (post-thyroid/parathyroid surgery — most common acute cause)
- Vitamin D deficiency / osteomalacia
- Hypomagnesaemia (magnesium required for PTH secretion and action)
- Acute pancreatitis, rhabdomyolysis
- CKD (reduced vitamin D activation)
- Massive blood transfusion (citrate chelates calcium)
- Drugs: bisphosphonates, denosumab, furosemide, phenytoin, cisplatin
Hypercalcaemia
Corrected Ca²⁺ >2.6 mmol/L · IV saline · Zoledronate · Malignancy · Hyperparathyroidism
BNF · NICE CKSHypercalcaemic crisis (Ca²⁺ >3.5 mmol/L or severe symptoms) → aggressive IV saline + zoledronate + dialysis if refractory. ICU/HDU setting.
Mild (2.6–3.0)
"Bones, stones, groans, thrones, moans." Fatigue, constipation, polyuria. Identify cause. Hydration.
Moderate (3.0–3.5)
Nausea, confusion, muscle weakness, ECG changes (short QT). IV saline + bisphosphonate.
Severe (>3.5 / Crisis)
Coma, cardiac arrhythmias, acute pancreatitis, renal failure. ICU. Aggressive saline + dialysis.
- Bones: bone pain, fractures, osteitis fibrosa cystica
- Stones: renal calculi (calcium oxalate/phosphate), nephrocalcinosis
- Groans: abdominal pain, constipation, pancreatitis, peptic ulcer
- Thrones: polyuria, polydipsia, dehydration
- Moans: fatigue, depression, confusion, psychosis
| Category | Causes | PTH |
|---|---|---|
| Primary hyperparathyroidism (most common overall) | Adenoma (80%), hyperplasia, carcinoma | ↑ or inappropriately normal |
| Malignancy (most common in hospital) | PTHrP (squamous/renal/breast), bone mets, myeloma, lymphoma | ↓ |
| Vitamin D toxicity / granulomata | Sarcoidosis, TB, vitamin D overdose | ↓ |
| Drugs | Thiazides, lithium, milk-alkali syndrome, vitamin A | ↑ (lithium/thiazides) |
Hypomagnesaemia
Mg²⁺ <0.7 mmol/L · Arrhythmias · Tetany · IV MgSO₄ · Often with hypokalaemia/hypocalcaemia
BNF · NICE CKSHypomagnesaemia causes refractory hypokalaemia and hypocalcaemia — correct Mg²⁺ first before potassium/calcium will respond to replacement.
- Neuromuscular: tremor, tetany, muscle weakness, Trousseau/Chvostek signs (due to concurrent hypocalcaemia)
- Cardiac: palpitations, ventricular arrhythmias, Torsades de Pointes, AF
- ECG: prolonged QT, broad T waves, ST changes
- CNS: confusion, seizures, nystagmus, ataxia
- GI losses: diarrhoea (most common), vomiting, NG drainage, short bowel syndrome, malabsorption
- Renal losses: loop/thiazide diuretics, cisplatin, amphotericin, aminoglycosides, PPI use (chronic)
- Alcohol excess (poor intake + renal wasting)
- Refeeding syndrome
- Hyperaldosteronism, hyperthyroidism, hyperparathyroidism
50% of infused Mg²⁺ is excreted renally. Multiple doses needed. Check Mg²⁺ daily during IV replacement. If renal impairment: reduce dose and frequency — risk of hypermagnesaemia.
Hypermagnesaemia
Mg²⁺ >1.1 mmol/L · Rare · Usually iatrogenic or renal failure · Calcium gluconate · Dialysis
BNF · RCOG 2022 (eclampsia)Mg²⁺ >2.5: respiratory depression, complete heart block, cardiac arrest. Stop all magnesium. Give calcium gluconate immediately. Dialysis if renal failure.
| Mg²⁺ Level | Clinical Features |
|---|---|
| 1.1–2.0 mmol/L (mild) | Nausea, flushing, warmth, headache |
| 2.0–2.5 mmol/L (moderate) | Hypotension, bradycardia, somnolence, absent deep tendon reflexes |
| 2.5–5.0 mmol/L (severe) | Respiratory depression, complete heart block, ileus |
| >5.0 mmol/L (critical) | Respiratory arrest, cardiac arrest |
- Iatrogenic: excessive IV MgSO₄ (eclampsia treatment, TPN, antacid overuse)
- Renal failure (impaired excretion — even normal intake)
- Excessive oral antacid/laxative use (Mg-containing: Milk of Magnesia, Gaviscon)
Hypophosphataemia
PO₄ <0.8 mmol/L · Refeeding syndrome · Respiratory failure · IV/oral phosphate
NICE NG22 (Refeeding) · BNFSevere hypophosphataemia (<0.3 mmol/L): respiratory muscle weakness, respiratory failure, rhabdomyolysis, haemolysis, cardiac dysfunction, encephalopathy. IV replacement urgently.
Mild (0.6–0.8)
Often asymptomatic. Oral phosphate replacement. Treat cause.
Moderate (0.3–0.6)
Muscle weakness, fatigue, bone pain, paraesthesia. Oral ± IV phosphate.
Severe (<0.3)
Respiratory failure, encephalopathy, haemolysis, rhabdomyolysis. IV phosphate urgently.
- Refeeding syndrome (most important — re-initiation of nutrition after starvation → insulin surge → cellular uptake)
- Malabsorption, prolonged NG drainage
- Antacid use (aluminium/calcium-based antacids bind phosphate)
- Alcoholism, poor intake
- Hyperparathyroidism, vitamin D deficiency
- Drugs: insulin excess, salbutamol, TPN without phosphate, diuretics
Hyperphosphataemia
PO₄ >1.5 mmol/L · CKD · Tumour lysis · Phosphate binders · Dialysis
NICE NG203 (CKD) · BNF- CKD (most common — impaired renal phosphate excretion)
- Hypoparathyroidism (reduced phosphaturic effect of PTH)
- Rhabdomyolysis, tumour lysis syndrome
- Excess phosphate intake (phosphate-containing enemas, laxatives, enteral feeds)
- Acidosis (shifts phosphate extracellularly)
- Hypocalcaemia (phosphate binds calcium → symptomatic tetany)
- Calcification of soft tissues, vessels (vascular calcification)
- Secondary hyperparathyroidism in CKD
- Renal osteodystrophy (long-term)
Tumour Lysis Syndrome (TLS)
Cairo-Bishop Criteria · Rasburicase · Allopurinol · Aggressive hydration · Dialysis
BCSH / ESMO Guidelines 2016TLS is an oncological emergency. Massive cell death releases K⁺, PO₄, uric acid, causing hyperkalaemia, hyperphosphataemia, hypocalcaemia, hyperuricaemia, and AKI. Can cause fatal arrhythmia within hours.
| Parameter | Threshold |
|---|---|
| Uric acid | ≥476 μmol/L or 25% increase from baseline |
| Potassium | ≥6.0 mmol/L or 25% increase |
| Phosphate | ≥1.45 mmol/L or 25% increase |
| Calcium (corrected) | ≤1.75 mmol/L or 25% decrease |
- Creatinine ≥1.5 × ULN (AKI)
- Cardiac arrhythmia / sudden death
- Seizures
- Burkitt lymphoma, B-cell ALL (highest risk)
- Diffuse large B-cell lymphoma (DLBCL)
- AML with high WBC count
- CLL treated with venetoclax
- Any bulky disease or high proliferative index
- 1Aggressive IV hydration — immediately. Do NOT wait for TLS to develop.
- 2Rasburicase or allopurinol to lower uric acid (see doses below).
- 3Treat hyperkalaemia, hyperphosphataemia, hypocalcaemia as per respective protocols.
- 4Continuous cardiac monitoring — arrhythmia risk from hyperkalaemia/hypocalcaemia.
- 5Strict urine output monitoring — target UO >100 mL/h (2 mL/kg/h). Catheter.
- 6Bloods every 4–6h: U&E, Ca²⁺, PO₄, uric acid, LDH, creatinine.
- 7If AKI develops or electrolytes refractory: emergency haemodialysis. Contact renal team early.
Neutropenic Sepsis
NICE NG151 (2023) · Neutrophils <0.5 × 10⁹/L + fever/sepsis · Piperacillin-tazobactam · G-CSF
NICE NG151 · 2023NICE NG151: Start antibiotics within 60 minutes of presentation. Neutropenic sepsis carries >10% mortality if untreated. Do NOT wait for culture results. Call oncology.
- Neutrophil count <0.5 × 10⁹/L (or expected to fall to <0.5 within 48h)
- AND fever (temperature >38°C), OR other signs of sepsis (rigors, hypotension, tachycardia)
- In context of recent chemotherapy (usually within 2–3 weeks) or haematological malignancy
Neutropenic patients may NOT mount a fever — any symptom of infection in a neutropenic patient should be treated as neutropenic sepsis. Classical signs of infection (localising tenderness, pus) may be absent.
| Feature | Score |
|---|---|
| Burden of illness — no/mild symptoms | 5 |
| No hypotension (SBP >90) | 5 |
| No COPD | 4 |
| Solid tumour or no prior fungal infection | 4 |
| No dehydration | 3 |
| Outpatient at onset | 3 |
| Age <60 | 2 |
- FBC with differential, CRP, U&E, LFTs, LDH, coagulation
- Blood cultures ×2 sets — peripheral AND central line (if present) before antibiotics if possible, but do not delay antibiotics
- Urine MC&S, CXR
- Throat/nasal swabs, stool if diarrhoea (C.diff, viral)
- CMV/EBV/HSV PCR if prolonged fever
- CT chest/abdomen/pelvis if fever >72–96h — looking for occult source, fungal pneumonia (ground-glass, halo sign)
Rhabdomyolysis
CK >1000 IU/L · Myoglobinuria · Aggressive IV fluids · AKI prevention · Compartment syndrome
BNF · NICE CKS · UpToDate 2024Massive CK rise + tea/cola-coloured urine = rhabdomyolysis. Aggressive IV saline is the cornerstone — target UO 200–300 mL/h. AKI is the main life-threatening complication.
- Muscle pain, weakness, tenderness (may be absent in 50%)
- Dark brown "tea/cola-coloured" urine (myoglobinuria)
- Markedly elevated CK (>1000 IU/L — significant; >5000 IU/L — severe)
- Trauma/crush injury, prolonged immobility, burns
- Run/exertion (exertional rhabdomyolysis, marathon, seizures)
- Alcohol, drugs of abuse (cocaine, heroin, MDMA, amphetamines)
- Urinalysis — dipstick positive for "blood" but no RBCs (myoglobinuria)
- Medications — statins, fibrates, antipsychotics, suxamethonium
- Acute illness — extreme hyperthermia (sepsis, NMS, malignant hyperthermia, heatstroke)
- CK (serial — peak at 24–72h, then decline)
- U&E, creatinine (AKI), LFTs
- K⁺, Ca²⁺, PO₄ (electrolyte complications)
- Urine dipstick (blood positive without RBCs), urinalysis, urine myoglobin
- Coagulation screen (DIC risk)
- Troponin (myocardial involvement), ABG
Compartment Syndrome: Suspect if severe swollen, tense compartment + severe pain + paraesthesia/weakness. Urgent surgical review — fasciotomy may be needed. Pressures >30 mmHg or >20 mmHg below diastolic BP → fasciotomy.
Addisonian Crisis (Acute Adrenal Insufficiency)
NICE CG128 / Society for Endocrinology 2020 · Hydrocortisone 100 mg IV · Fluids · Glucose
NICE CG128 · Endocrine Society 2020Do NOT wait for cortisol results before treating if clinical picture consistent with adrenal crisis. Hydrocortisone 100 mg IV immediately. Delay is fatal. Take blood for cortisol/ACTH first if <2 min delay, but do not delay treatment otherwise.
Acute Presentation
Profound hypotension, shock, cardiovascular collapse unresponsive to fluids/vasopressors. Hyponatraemia, hyperkalaemia, hypoglycaemia.
Subacute Symptoms
Fatigue, weakness, anorexia, nausea, vomiting, abdominal pain, myalgias. Weight loss. Often precipitated by illness/surgery.
- Hyponatraemia (most common — aldosterone deficiency → Na⁺ wasting)
- Hyperkalaemia (aldosterone deficiency → K⁺ retention)
- Hypoglycaemia (cortisol required for gluconeogenesis)
- Raised creatinine, eosinophilia, lymphocytosis on FBC
- Low morning cortisol (<100 nmol/L very suggestive; <500 nmol/L with acute illness warrants treatment)
- Elevated ACTH in primary adrenal failure; low in secondary (pituitary)
- Infection (most common trigger — gastroenteritis, pneumonia, UTI)
- Surgery, trauma, procedure
- Missed/insufficient steroid dosing
- Drugs that increase steroid metabolism: rifampicin, phenytoin, carbamazepine
- Bilateral adrenal haemorrhage (Waterhouse-Friderichsen: meningococcal sepsis)
- Pituitary apoplexy (secondary adrenal failure)
- 1Take blood for cortisol and ACTH immediately (before steroids if <2 min delay). DO NOT DELAY treatment.
- 2Hydrocortisone 100 mg IV bolus immediately.
- 3IV fluid resuscitation: 0.9% NaCl 1 L over 30–60 min then reassess (avoid hypotonic/dextrose-only fluids).
- 4Check BM — treat hypoglycaemia with IV dextrose 10% 150–200 mL if BG <4 mmol/L.
- 5Continue Hydrocortisone 100 mg IV/IM q6–8h (or CSCI 200 mg/24h) for first 24–48h.
- 6Identify and treat the precipitating cause (e.g., antibiotics for infection).
- 7Monitor U&E, BG, BP 4-hourly. ICU/HDU if haemodynamically unstable.
- 8Endocrinology review. Educate patient on sick day rules and steroid emergency card.
| Test | Finding in Adrenal Insufficiency |
|---|---|
| Morning cortisol (9am) | <100 nmol/L: highly suggestive. <500 with acute illness: treat empirically |
| ACTH (plasma) | ↑ Primary (adrenal gland problem); ↓ Secondary (pituitary/hypothalamic) |
| Short synacthen test (250 mcg ACTH IM) | Cortisol <550 nmol/L at 30–60 min = abnormal (confirmed diagnosis) |
| Na⁺/K⁺ | Hyponatraemia + hyperkalaemia (primary); hyponatraemia without hyperkalaemia (secondary) |
| Adrenal antibodies | 21-hydroxylase antibodies in autoimmune Addison's (80%) |
| CT adrenals | Adrenal enlargement (TB, metastases, haemorrhage), atrophy (autoimmune) |
Bradyarrhythmias & Complete Heart Block
RCUK 2021 · NICE NG241 · Atropine · Transcutaneous pacing · Isoprenaline · Transvenous pacing
RCUK 2021 · NICE NG241Haemodynamically unstable bradycardia (SBP <90, GCS↓, chest pain, acute HF, syncope) → atropine immediately. If no response: transcutaneous pacing NOW. Do not delay.
First Degree AV Block
PR >200 ms. No haemodynamic compromise. Monitor. Identify and treat cause. No intervention needed.
Second Degree — Mobitz I (Wenckebach)
Progressive PR lengthening then dropped QRS. Usually benign/inferior MI. Monitor. Treat if symptomatic.
Second Degree — Mobitz II
Fixed PR with sudden dropped QRS. Unstable — risk of progression to CHB. Pacing often required.
Third Degree (Complete Heart Block)
Complete AV dissociation. P waves and QRS independent. Escape rhythm 20–40 bpm. Emergency pacing.
- Shock: SBP <90 mmHg, pallor, cold clammy, diaphoresis
- Syncope or pre-syncope
- Myocardial ischaemia (chest pain, ischaemic ECG changes)
- Acute heart failure (pulmonary oedema)
- Heart rate <40 bpm (higher rates may still be haemodynamically significant if symptomatic)
Risk of asystole: Consider immediate pacing (do not wait for adverse features) if: recent asystole, Mobitz II block, CHB with broad complex escape, ventricular pause >3 sec.
- 112-lead ECG. IV access. Continuous monitoring. Identify and treat reversible causes.
- 2If no adverse features and low risk of asystole: observe, treat cause, cardiology review.
- 3If adverse features present: Atropine 500 mcg IV — first-line immediately.
- 4Repeat atropine 500 mcg IV every 3–5 min up to maximum 3 mg total.
- 5If atropine ineffective or CHB/Mobitz II: Transcutaneous pacing (TCP) immediately.
- 6Whilst preparing TCP or as bridge: Isoprenaline infusion or Adrenaline infusion (see doses).
- 7Arrange urgent transvenous cardiac pacing — cardiology/catheter lab. TCP is a bridge only.
- 8Identify and treat reversible causes: inferior MI (reperfusion), hyperkalaemia, drug toxicity (digoxin, beta-blocker, CCB, amiodarone), Lyme disease, hypothyroidism.
- CHB (complete heart block) with haemodynamic compromise
- Symptomatic Mobitz II not responding to atropine
- Asystole with P waves (standby pacing)
- Bilateral bundle branch block with PR prolongation (high risk of CHB)
- Post-anterior MI with new RBBB + LAHB/LPHB (high risk)
- As bridge to permanent pacemaker implantation
Access: right internal jugular or subclavian preferred. Femoral usable but higher displacement risk. Aim for RV apex. Check capture threshold and set output at 2× threshold. Secure lead position fluoroscopically or via ECG guidance. Cardiology-led procedure.
Aortic Dissection
Stanford A vs B · ESC 2014/2023 · Aggressive BP & HR control · Surgical vs endovascular · NICE guidance
ESC 2023 · NICEType A aortic dissection (ascending aorta involved) = surgical emergency. Mortality ~1–2% per hour untreated. Immediate cardiothoracic surgery referral. While awaiting: target SBP 100–120 mmHg, HR <60 bpm with IV labetalol/esmolol.
Stanford Type A
Involves ascending aorta (±arch, descending). ~65% of cases. Surgical emergency. Mortality >25% in 24h without surgery.
Stanford Type B
Descending aorta only (distal to left subclavian). ~35%. Medical management unless complicated (ischaemia, rupture, rapid expansion) → TEVAR.
- Sudden-onset severe "tearing" or "ripping" chest/back pain — maximal at onset
- Pain may radiate to back, abdomen, or legs as dissection propagates
- Pulse deficit or BP differential >20 mmHg between arms (30–40% sensitivity)
- Aortic regurgitation murmur (Type A — 40–50%)
- Neurological deficit (stroke, paraplegia — spinal artery involvement)
- Haemodynamic shock (Type A — pericardial tamponade, severe AR)
- Normal CXR does NOT exclude dissection — 15–20% have normal CXR
| High-risk Feature | Score |
|---|---|
| High-risk conditions: Marfan's, aortic disease, family history, known aortic valve, recent aortic procedure | 1 |
| High-risk pain: abrupt onset, severe, tearing/ripping/sharp character | 1 |
| High-risk exam: BP differential >20 mmHg, pulse deficit, focal neuro deficit, aortic regurgitation, hypotension/shock | 1 |
- 1ECG (MI, arrhythmia — Type A can occlude coronary ostia).
- 2CXR: widened mediastinum (>8 cm), loss of aortic knuckle, pleural effusion (left), tracheal deviation.
- 3CT aorta with contrast (CT angiography) — gold standard. Full aorta from root to iliacs. Identifies extent, branch involvement, true/false lumen.
- 4Bloods: FBC, U&E, coagulation, G&S, troponin, D-dimer (only if ADD-RS 0), lactate, LFTs.
- 5Bedside echo (POCUS): pericardial effusion/tamponade, AR, aortic root dilatation — useful while awaiting CT.
- 6BP in both arms simultaneously. Check all peripheral pulses.
If dissection reaches coronary ostia → inferior STEMI pattern on ECG. Do NOT thrombolyse. ECG ischaemic changes in suspected dissection mandate CT aorta before any reperfusion strategy.
Targets (ESC 2023): SBP 100–120 mmHg AND heart rate <60 bpm. Reducing dP/dt (rate of pressure rise) is critical — use beta-blocker FIRST, then add vasodilator if needed. Never vasodilate without beta-blockade (reflex tachycardia worsens dissection).
| Type | Treatment | Urgency |
|---|---|---|
| Type A (uncomplicated) | Emergency open surgery (Bentall/ascending aorta replacement) | Immediate — minutes to hours |
| Type A + tamponade | Pericardiocentesis only if PEA/haemodynamic collapse as bridge — NOT routine (can worsen by increasing BP and propagating dissection) | Surgery is definitive |
| Type B (uncomplicated) | Medical management alone (BP/HR control) | Admit HDU/ICU — 7–14 days |
| Type B (complicated)* | TEVAR (Thoracic Endovascular Aortic Repair) | Urgent — within 24h |
Cardiac Tamponade
Beck's triad · Pulsus paradoxus · Pericardiocentesis · POCUS-guided · Surgical drainage
ESC 2015 · RCEM · ATLSTamponade causing PEA arrest: immediate needle pericardiocentesis without USS guidance. Tamponade with severe haemodynamic compromise: USS-guided pericardiocentesis ASAP. Do NOT delay for formal echo.
Beck's Triad
1. Hypotension (low cardiac output)
2. Raised JVP (obstructed venous return)
3. Muffled heart sounds
All three present in only ~30% — high index of suspicion needed.
Pulsus Paradoxus
Inspiratory ↓ in SBP >10 mmHg during normal breathing. Measure with sphygmomanometer. Sensitive but not specific.
ECG Features
Sinus tachycardia (most common). Low voltage QRS. Electrical alternans (alternating QRS axis — pathognomonic when present). PR depression.
CXR Features
Enlarged globular cardiac silhouette ("water bottle heart") if chronic/large effusion. May be normal in acute/small tamponade.
- Trauma — penetrating chest injury (most acute)
- Malignancy — lung, breast, lymphoma (most common overall)
- Pericarditis (viral, autoimmune)
- Aortic dissection Type A (haemopericardium)
- Post-cardiac surgery / intervention (CABG, PCI, pacemaker lead)
- Uraemia (renal failure)
- Hypothyroidism (myxoedema)
- Drugs: hydralazine, procainamide (lupus-like)
POCUS findings: Pericardial effusion + RV collapse in early diastole (most sensitive sign) + RA collapse + IVC plethora (non-collapsing with inspiration >50%) + exaggerated respiratory variation in mitral/tricuspid flow.
- 1High-flow O₂, IV access ×2, continuous monitoring. Call cardiology/cardiothoracic urgently.
- 2Bedside POCUS — confirm effusion and haemodynamic significance.
- 3IV fluid bolus 250–500 mL 0.9% NaCl — temporising measure to maintain preload (limited benefit, do not over-fluid).
- 4Avoid vasodilators, diuretics (reduce preload → catastrophic).
- 5If haemodynamically compromised: USS-guided pericardiocentesis immediately.
- 6PEA arrest with suspected tamponade: immediate blind pericardiocentesis or thoracotomy.
- 7Traumatic haemopericardium → emergency thoracotomy (pericardiocentesis insufficient for haemorrhage control).
Intubation risk: Avoid intubation/general anaesthesia in tamponade if possible — loss of sympathetic tone with induction can cause immediate cardiac arrest. If essential: awake intubation or perform pericardiocentesis before induction.
Eclampsia & Hypertension in Pregnancy
RCOG GTG 10A (2022) · NICE NG133 · MgSO₄ · Labetalol · Hydralazine · Delivery
RCOG GTG10A 2022 · NICE NG133Eclamptic seizure: MgSO₄ 4 g IV over 5 min immediately. Call obstetric/anaesthetic team. Aim delivery after stabilisation — delivery is the only cure. HELLP syndrome: urgent haematology + obstetric input.
Gestational Hypertension
BP ≥140/90 mmHg after 20 weeks. No proteinuria or other features. Monitor closely. Treat if BP ≥150/100.
Pre-eclampsia
BP ≥140/90 + proteinuria (PCR ≥30 mg/mmol) OR end-organ dysfunction. After 20 weeks.
Severe Pre-eclampsia
SBP ≥160 or DBP ≥110 mmHg OR end-organ dysfunction (renal, hepatic, neuro, haematological).
Eclampsia
Tonic-clonic seizures in pre-eclampsia. Can occur antepartum (38%), intrapartum (18%), postpartum (44% — up to 4 weeks).
- Haemolysis (↑LDH, ↑bilirubin, fragmented red cells on film)
- Elevated Liver enzymes (ALT/AST >70 IU/L)
- Low Platelets (<100 × 10⁹/L)
- Associated with pre-eclampsia; may occur without hypertension; carries significant maternal mortality
- Severe headache (not relieved by paracetamol)
- Visual disturbances (blurred vision, flashing lights, scotomata)
- Right upper quadrant / epigastric pain
- Nausea and vomiting, rapidly worsening oedema
- Papilloedema, hyperreflexia, clonus (>3 beats)
If eclamptic seizure does not respond to MgSO₄: Diazepam 10 mg IV or Lorazepam 4 mg IV as second-line. Anaesthetic team for RSI if refractory. Rule out other causes (stroke, epilepsy, metabolic).
Treatment threshold (NICE NG133 updated 2023): Treat BP ≥140/90 mmHg in pregnancy. Treat immediately if BP ≥160/110 — aim SBP 130–150 mmHg and DBP 80–100 mmHg. Do NOT lower below 130/80 (uteroplacental insufficiency).
- Delivery is the definitive treatment — stabilise mother first, then deliver
- Timing: >37 weeks severe pre-eclampsia → deliver. 34–37 weeks → discuss risks/benefits. <34 weeks → consider corticosteroids (foetal lung maturity) then deliver if unable to stabilise
- Corticosteroids (foetal lung maturity): Betamethasone 12 mg IM × 2 doses 24h apart (if <34+6 weeks and delivery likely within 7 days)
- Fluid balance: restrict to 80 mL/h IV unless haemorrhage — risk of pulmonary oedema
- Foetal monitoring: CTG continuously in severe pre-eclampsia
- HELLP: platelet transfusion if PLT <50 before delivery; FFP if coagulopathy
- Postpartum monitoring: continue MgSO₄ for 24h post-delivery; BP may worsen in first 3–5 days
- Postpartum antihypertensives: Enalapril (safe in breastfeeding) or Nifedipine MR
Pneumothorax
BTS Guideline 2023 · Tension · Primary vs Secondary · Needle aspiration · Chest drain · Heimlich valve
BTS 2023 · RCEMTension pneumothorax = clinical diagnosis — do NOT wait for CXR. Tracheal deviation away, absent breath sounds, haemodynamic collapse → immediate large-bore needle decompression 2nd ICS MCL. Then chest drain.
Tension Pneumothorax
One-way valve mechanism. Progressive pressure build-up. Cardiovascular collapse. Clinical diagnosis — immediate needle decompression. Most common post-trauma, ventilated patients.
Primary Spontaneous (PSP)
No underlying lung disease. Young, tall, thin males. Smoking risk factor. Often small/moderate. BTS: usually treat conservatively if stable.
Secondary Spontaneous (SSP)
Underlying lung disease (COPD most common). Higher morbidity — poor reserve. Most require intervention. Lower threshold for admission and drainage.
Iatrogenic / Traumatic
CVC insertion, lung biopsy, chest trauma, rib fractures. Haemopneumothorax in trauma. Drain required if ventilated.
| Measurement | Definition |
|---|---|
| Small | <2 cm rim of air at level of hilum on CXR (or <2 cm from chest wall at apex on CXR) |
| Large | ≥2 cm rim of air at level of hilum |
| CT-based | CT preferred for accurate sizing; <2 cm apex-to-cupola distance on CT = small |
BTS 2023 key change: Conservative management (ambulatory) preferred for ALL stable PSP — even large — unless haemodynamically compromised. Avoid routine needle aspiration for large PSP if stable. Heimlich valve ambulatory device preferred over inpatient drain in suitable patients.
All SSP patients should be admitted. Even small SSP in COPD can be life-threatening. Lower threshold for chest drain insertion. High-flow O₂ if no CO₂ retention risk (accelerates resolution by nitrogen washout).
- Small-bore (8–14F Seldinger drain) preferred for spontaneous pneumothorax (BTS 2023)
- Do not clamp drains with ongoing air leak
- Bubbling stops = lung re-expanded. Confirm CXR before removal.
- Persistent air leak >5–7 days → thoracic surgery referral (video-assisted thoracoscopic surgery, VATS)
- Pleurodesis: consider after second ipsilateral PSP or first SSP in high-risk patients
- Recurrence rate: PSP ~30% at 5 years; SSP higher
Massive Haemoptysis
BTS / ERS Guideline · >200–300 mL/24h or life-threatening airway bleeding · BAE · Rigid bronchoscopy · Positioning
BTS / ERS · RCEMImmediate airway control is priority. Position patient with bleeding lung dependent (bleeding-side down) to protect contralateral lung. Death is from asphyxiation, not exsanguination. Call respiratory/IR/thoracics urgently.
Mild/Non-massive
<100 mL/24h. Common. Usually from bronchitis, infection, PE. Investigate, outpatient if stable.
Significant
100–200 mL/24h. Admit. Active investigation. CT angiography.
Massive / Life-threatening
>200–300 mL/24h (varies by definition) OR any amount compromising airway/haemodynamics. Immediate intervention required.
- Bronchiectasis (most common in developed world — including CF)
- Lung cancer (primary or metastatic)
- Tuberculosis (active or post-primary cavity, Rasmussen aneurysm)
- Fungal infection (aspergilloma — mycetoma in cavity)
- Pulmonary embolism
- Pulmonary arteriovenous malformation (PAVM)
- Mitral stenosis (pulmonary hypertension)
- Vasculitis (GPA/Wegener's, Goodpasture's, SLE)
- Trauma, iatrogenic (post-procedure)
- 1Position patient with bleeding lung DEPENDENT (bleeding side down) — prevents blood flooding contralateral lung. If lateralisation unknown, place semi-recumbent.
- 2High-flow O₂ 15 L/min via NRB mask. Aim SpO₂ ≥94%.
- 3IV access ×2 large-bore. Bloods: FBC, coagulation, crossmatch, U&E, ABG.
- 4Correct coagulopathy: FFP, platelets, PCC as needed. Stop anticoagulants.
- 5Tranexamic acid 1 g IV over 10 min (off-label but widely used — evidence from CRASH-3 extrapolated).
- 6CT chest with contrast / CT pulmonary angiography — identifies source and guides BAE.
- 7Urgent respiratory/thoracic surgery/interventional radiology referral.
- 8If airway compromised: RSI and intubation — consider selective intubation of unaffected bronchus (right main bronchus easier; left using long tube/fibreoptic).
Respiratory Failure
NICE NG38 (ARDS) · BTS NIV Guidelines 2016 · Type 1 vs Type 2 · HFNO · NIV · Intubation criteria
NICE NG38 · BTS 2016 · FICM 2021Type 1 — Hypoxaemic
PaO₂ <8 kPa (on air or supplemental O₂)
PaCO₂ normal or low
Problem: V/Q mismatch, shunt, diffusion failure
Causes: pneumonia, PE, pulmonary oedema, ARDS, pneumothorax, haemothorax
Type 2 — Hypercapnic
PaO₂ <8 kPa AND PaCO₂ >6 kPa
Problem: alveolar hypoventilation ± V/Q mismatch
Causes: COPD, acute severe asthma, neuromuscular disease, obesity hypoventilation, chest wall deformity, drug-induced (opioids, benzos)
| Parameter | Normal | Type 1 RF | Type 2 RF (acute) | Type 2 (chronic) |
|---|---|---|---|---|
| pH | 7.35–7.45 | Normal/↑ | ↓ (acidosis) | Normal (compensated) |
| PaO₂ (kPa) | 10–13 | <8 | <8 | <8 |
| PaCO₂ (kPa) | 4.5–6.0 | Normal/↓ | >6 ↑ | >6 (chronic↑) |
| HCO₃⁻ (mmol/L) | 22–26 | Normal | Normal/↑ early | ↑↑ (renal compensation) |
| A-a gradient | <2 kPa | ↑↑ | ↑ (if lung disease) | Variable |
BTS O₂ guideline: Target SpO₂ 94–98% in most patients. Target 88–92% in patients at risk of hypercapnic respiratory failure (COPD, obesity hypoventilation, neuromuscular disease). Hyperoxia is harmful.
| Device | FiO₂ Achieved | Indication |
|---|---|---|
| Nasal cannula 1–6 L/min | ~24–44% | Mild hypoxia, long-term use |
| Simple face mask 5–10 L/min | ~35–55% | Moderate hypoxia |
| NRB mask 15 L/min | ~85–95% | Severe hypoxia, Type 1 RF, CO poisoning |
| Venturi mask 24–60% | Fixed (24–60%) | COPD — controlled O₂ delivery |
| HFNO (Optiflow) up to 60 L/min | Up to 100% | Severe Type 1 RF, post-extubation, COVID-19 |
| CPAP / BiPAP (NIV) | Up to 100% | Type 1 (CPAP for APO) / Type 2 (BiPAP) |
- Failure of NIV or HFNO (PaO₂ <8 kPa on FiO₂ 0.6 / SpO₂ <90% despite maximal support)
- Worsening acidosis: pH <7.25 despite 1h NIV with rising PaCO₂
- Haemodynamic instability (SBP <90 mmHg, shock)
- Reduced GCS/inability to protect airway
- Respiratory arrest or imminent arrest
- Exhaustion — cannot sustain respiratory effort
- NIV failure: pH not improving after 1–2h of optimal BiPAP
ARDS Berlin Definition (NICE NG38): Acute onset <1 week, bilateral infiltrates on CXR/CT, not fully explained by cardiac failure/fluid overload, PaO₂/FiO₂ ratio: mild 200–300, moderate 100–200, severe <100 mmHg. Prone positioning for >12h/day in moderate-severe ARDS.
Raised Intracranial Pressure / Herniation
RCEM guidelines · NICE · Neurocritical Care Society
RCEM · NCS 2024Herniation is a clinical emergency. Do not delay treatment awaiting imaging if signs of transtentorial herniation are present. Neurosurgical referral immediately.
Early Raised ICP
Headache (worse lying flat/morning), vomiting, papilloedema, declining GCS, hypertension + bradycardia
Cushing's Triad
Hypertension + bradycardia + irregular respirations — late sign of impending herniation
Transtentorial Herniation
Unilateral fixed dilated pupil (CN III compression), contralateral hemiplegia, posturing, GCS ↓↓
Tonsillar Herniation
Sudden apnoea, bilateral fixed dilated pupils, cardiovascular collapse — imminent death
Do not perform LP if signs of raised ICP — risk of coning. CT head first. Discuss with neurosurgery if mass lesion / midline shift.
Meningitis / Encephalitis
NICE NG240 (2023) — bacterial meningitis & meningococcal disease · HSV encephalitis
NICE NG240 · 2023Do not delay antibiotics for LP. Treat empirically if clinical suspicion is high. Every hour of delay worsens outcome.
Meningism
Neck stiffness, Kernig's sign, Brudzinski's sign, photophobia, phonophobia, severe headache
Meningococcal Septicaemia
Non-blanching petechial/purpuric rash — treat as emergency. Sepsis, DIC, limb ischaemia
Encephalitis Features
Altered consciousness, seizures, focal neurology, personality change, fever — HSV until proven otherwise
When to CT Before LP
GCS <15, focal neuro signs, papilloedema, immunocompromised, seizures, coagulopathy
| Parameter | Bacterial | Viral | TB | Normal |
|---|---|---|---|---|
| Appearance | Turbid/purulent | Clear | Fibrin web / xanthochromic | Crystal clear |
| White cells | >1000 PMN/µL | 10–500 lymphocytes | 100–500 lymphocytes | <5/µL |
| Protein | >1 g/L | 0.5–1 g/L | >1 g/L | 0.15–0.45 g/L |
| Glucose (CSF:serum) | <0.6 / <50% | Normal | <0.5 | >0.6 |
| Opening pressure | Elevated | Normal/↑ | Elevated | 6–25 cmH₂O |
Waterhouse-Friderichsen Syndrome: Bilateral adrenal haemorrhage in severe meningococcal sepsis — presents with shock, DIC, purpuric rash. Add Hydrocortisone 100 mg IV QDS.
Guillain-Barré Syndrome (GBS)
RCEM · NICE · EAN Guidelines — IVIG, plasmapheresis, respiratory monitoring
EAN 2023 · RCEMRespiratory failure occurs in up to 30% — serial NIF/FVC monitoring is essential. Early ITU referral if FVC <20 mL/kg or deteriorating rapidly.
Myasthenic Crisis
RCEM · EAN Guidelines — differentiate cholinergic vs myasthenic crisis
EAN 2023 · RCEMMyasthenic crisis = life-threatening respiratory failure from NMJ dysfunction. Intubate early. FVC <15 mL/kg = imminent arrest.
| Feature | Myasthenic Crisis | Cholinergic Crisis |
|---|---|---|
| Cause | Undertreatment / infection / trigger | Excess anticholinesterase (pyridostigmine overdose) |
| Pupils | Normal / dilated | Miosis (small) |
| Secretions | Dry | SLUDGE: Salivation, Lacrimation, Urination, Defaecation, GI distress, Emesis |
| Fasciculations | Absent | Present |
| Bradycardia | No | Yes |
| Response to edrophonium | Improves | Worsens |
| Management | IVIG / plasmapheresis, increase pyridostigmine | STOP pyridostigmine, Atropine 0.6–1.2 mg IV |
Acute Alcohol Withdrawal / Delirium Tremens
NICE CG100 · SIGN 74 · CIWA-Ar protocol · Pabrinex · Chlordiazepoxide
NICE CG100 · SIGN 74Delirium tremens carries up to 5–10% mortality untreated. Seizures typically 12–48h after last drink. DTs peak 48–72h. Wernicke's encephalopathy is a concurrent emergency.
CIWA ≤9
Mild withdrawal — outpatient/ward management, PO chlordiazepoxide, monitor
CIWA 10–19
Moderate — admit, symptom-triggered benzodiazepine, CIWA monitoring 4-hourly
CIWA ≥20
Severe / DTs — HDU/ITU, IV benzodiazepines, Pabrinex, consider phenobarbital
Acute Liver Failure (ALF)
NICE · King's College Criteria · NAC · Transplant referral
NICE · EASL 2023 · King's CollegeALF = jaundice + coagulopathy (INR >1.5) + encephalopathy within 26 weeks in absence of pre-existing liver disease. Refer early to liver centre. Mortality without transplant up to 80% in fulminant cases.
| Type | Onset from Jaundice | Common Causes |
|---|---|---|
| Hyperacute | <7 days | Paracetamol OD, hepatitis A/B |
| Acute | 7–28 days | Hepatitis B, hepatitis E, drugs |
| Subacute | 4–26 weeks | Seronegative hepatitis, drugs, Wilson's disease |
Refer early to liver transplant centre — do not wait until all criteria met. Early discussion improves outcome. MELD score >30 also indicates high mortality.
Upper GI Bleeding (UGIB)
NICE NG141 (2016, updated 2023) · Glasgow-Blatchford · Rockford · Endoscopy timing
NICE NG141 · 2023Haematemesis or melaena with shock: call resuscitation team, 2 large-bore IVs, activate MHP if needed. Restrict transfusion target Hb 70–80 g/L (unless ACS/haemodynamically compromised).
| Variable | Score |
|---|---|
| BUN (mmol/L): 6.5–8.0 | 2 |
| BUN: 8.0–10.0 | 3 |
| BUN: 10.0–25.0 | 4 |
| BUN: ≥25 | 6 |
| Hb (men): 120–130 g/L | 1 |
| Hb (men): 100–120 g/L | 3 |
| Hb (men): <100 g/L | 6 |
| Hb (women): 100–120 g/L | 1 |
| Hb (women): <100 g/L | 6 |
| SBP 100–109 mmHg | 1 |
| SBP 90–99 mmHg | 2 |
| SBP <90 mmHg | 3 |
| Pulse ≥100 bpm | 1 |
| Melaena | 1 |
| Syncope | 2 |
| Liver disease | 2 |
| Heart failure | 2 |
Acute Pancreatitis
NICE NG104 (2018) · Glasgow / Ranson scoring · Fluid resuscitation · ERCP timing
NICE NG104 · 2018Assess severity within 48h using Glasgow or Ranson criteria. Severe acute pancreatitis (≥3 criteria) requires HDU/ITU admission. Early aggressive fluid resuscitation is the cornerstone of treatment.
Bowel Obstruction / Volvulus
RCSUK · RCEM · ACPGBI — Small vs large bowel · Conservative vs surgical management
RCSUK · ACPGBI 2022Signs of strangulation or perforation (peritonism, sepsis, fever, lactate rise) require emergency surgery. Do not delay for further investigations if clinical signs of ischaemia.
Mesenteric Ischaemia
ESVS 2024 Guidelines · RCEM — Acute arterial, venous, non-occlusive subtypes
ESVS 2024 · RCEMMesenteric ischaemia has >60% mortality. "Pain out of proportion to examination" is the classic presentation. Any suspicion → immediate CT angiography + vascular surgery referral. Do not delay for clinical reassessment.
| Subtype | Proportion | Mechanism | Risk Factors |
|---|---|---|---|
| Acute SMA Embolism | 50% | Cardiac embolus (AF, MI, valve disease) | AF, endocarditis, post-MI mural thrombus |
| Acute SMA Thrombosis | 25% | Thrombus on pre-existing atherosclerosis | Atherosclerosis, previous CVD, smoking |
| Non-occlusive (NOMI) | 20% | Low-flow state — splanchnic vasoconstriction | Shock, cardiac failure, vasopressors, dialysis |
| Mesenteric Venous Thrombosis | 5–10% | Thrombosis of SMV/portal vein | Hypercoagulable states, cirrhosis, malignancy, OCP |
Portal venous gas or pneumatosis intestinalis on CT = bowel infarction — mortality >75%. Emergency surgery without delay.
Acute Kidney Injury (AKI)
NICE NG148 (2019) · KDIGO 2012 staging · Contrast nephropathy · Haemofiltration indications
NICE NG148 · KDIGO 2012AKI is present in up to 15% of hospital admissions and carries significant morbidity. Identify and remove the cause. Optimise fluid status. Avoid nephrotoxins. Early nephrology referral for KDIGO stage 3 or oliguria not responding to fluids.
| Stage | Serum Creatinine | Urine Output | Action |
|---|---|---|---|
| Stage 1 | ×1.5–1.9 baseline, or ↑≥26 µmol/L in 48h | <0.5 mL/kg/h for 6–12h | Identify cause, stop nephrotoxins, optimise fluids |
| Stage 2 | ×2.0–2.9 baseline | <0.5 mL/kg/h for ≥12h | As above + nephrology input, consider RRT |
| Stage 3 | ×3.0 baseline, or creatinine ≥354 µmol/L with acute rise ≥44, or RRT started | <0.3 mL/kg/h for ≥24h, or anuria ≥12h | Urgent nephrology referral, RRT likely |
Baseline creatinine: use lowest recorded in past 3 months or estimate using CKD-EPI/MDRD from age/sex (NICE NG148). AKI-24 alert: electronic alerting mandatory in NHS since 2014.
Pre-renal (60–70%)
Hypovolaemia (haemorrhage, diarrhoea, vomiting), sepsis, cardiac failure, hepatorenal syndrome, NSAIDs/ACEi/ARBs
Intrinsic (25–40%)
ATN (ischaemia, nephrotoxins), glomerulonephritis, vasculitis, interstitial nephritis (drugs), rhabdomyolysis, haemolysis
Post-renal (<5%)
BPH, prostate/cervical cancer, renal calculi (bilateral or solitary kidney), bladder neck obstruction, retroperitoneal fibrosis
Renal Stone / Ureteric Colic
NICE NG118 (2019) · RCEM · EAU Guidelines — analgesia, imaging, urology referral
NICE NG118 · EAU 2024Infected obstructed kidney = urological emergency. Sepsis + ureteric obstruction → emergency decompression (nephrostomy or ureteric stent) regardless of stone size.
Pyelonephritis
NICE NG111 (2018, updated 2022) · RCEM — antibiotics, sepsis criteria, imaging indications
NICE NG111 · 2022Pyelonephritis presenting with sepsis, deteriorating despite treatment, or structural abnormality requires USS/CT renal tract to exclude obstructed infected kidney — a urological emergency requiring immediate decompression.
Urological Emergencies
RCSUK · BAUS · EAU Guidelines — Testicular torsion, priapism, Fournier's gangrene, phimosis/paraphimosis, obstructive uropathy
RCSUK · BAUS 2024 · EAUTesticular torsion is a surgical emergency. Viable testis: >90% if operated within 6h; <10% if >24h. Do NOT delay surgery for USS if clinical suspicion is high.
Mortality 20–40%. Surgical debridement within hours is life-saving. Do not delay for imaging if clinical diagnosis is clear. Immediate urology/colorectal/plastics + ITU.
Sickle Cell Crisis
NICE NG143 (2021) · RCEM · BSH — vaso-occlusive, acute chest syndrome, exchange transfusion
NICE NG143 · BSH 2021Acute chest syndrome (ACS) = new pulmonary infiltrate + respiratory symptoms in sickle cell disease. Mortality up to 3%. Exchange transfusion indicated for severe ACS. Contact haematology immediately.
Vaso-occlusive Crisis (VOC)
Most common. Severe pain — bones (long bones, back, chest), abdomen. Precipitated by infection, cold, dehydration, hypoxia
Acute Chest Syndrome
New infiltrate on CXR + fever and/or respiratory symptoms. Can be rapidly fatal. Exchange transfusion indicated
Aplastic Crisis
Parvovirus B19 suppresses erythropoiesis → sudden severe anaemia (Hb drops 2–3 g/dL). Reticulocytopenia. Requires transfusion
Splenic Sequestration
Sudden spleen enlargement with pooling of blood. Acute anaemia + thrombocytopaenia. Exchange/simple transfusion urgently
Stroke / TIA
20% of SCD patients. Exchange transfusion (not simple top-up). Urgent CT head. Hydroxyurea + transfusion programme
Priapism
Ischaemic — treat per priapism protocol. Aspiration + phenylephrine. Exchange transfusion if prolonged (>4h)
Hyperviscosity Syndrome
BSH · BCSH Guidelines — myeloma, Waldenström's, leucostasis, plasmapheresis
BSH · BCSH 2023Hyperviscosity is a medical emergency. Plasmapheresis can be life-saving within hours. Contact haematology immediately. Do not transfuse red cells — increases viscosity further.
Superior Vena Cava (SVC) Obstruction
NICE NG234 · RCEM · NICE NG12 — dexamethasone, stenting, radiotherapy, chemotherapy
NICE NG234 · 2023SVC obstruction is rarely immediately life-threatening unless laryngeal/cerebral oedema present. Urgent oncology referral. Endovascular stenting is the fastest way to relieve symptoms.
Immune Thrombocytopaenia (ITP) with Severe Bleeding
BSH ITP Guidelines (2023) · RCEM — IVIG, steroids, platelet transfusion, anti-D, emergency splenectomy
BSH 2023 · RCEMITP with intracranial haemorrhage or life-threatening bleeding: simultaneous IVIG + platelet transfusion + IV methylprednisolone. Contact haematology immediately.
Platelets >50 × 10⁹/L
Usually asymptomatic. Monitor. No treatment unless surgery/procedure planned
Platelets 20–50 × 10⁹/L
Minor mucosal bleeding. Consider treatment if symptomatic or lifestyle compromised
Platelets 10–20 × 10⁹/L
Increased bleeding risk. Treat if symptomatic or planned procedure
Platelets <10 × 10⁹/L
High spontaneous bleeding risk. Treat. Wet purpura, mucosal bleeding, intracranial haemorrhage risk
Disseminated Intravascular Coagulation (DIC)
BSH DIC Guidelines (2009, updated 2021) · RCEM — FFP, cryoprecipitate, platelets, treat underlying cause
BSH 2021 · RCEMDIC is NOT a primary diagnosis — it is a consequence of an underlying condition. Treatment of the precipitating cause is the most important intervention. Supportive coagulation therapy bridges to definitive management.
| Parameter | DIC Finding | Comment |
|---|---|---|
| Platelets | ↓↓ (often <50) | Consumptive thrombocytopaenia |
| PT/INR | ↑↑ | Factor consumption |
| APTT | ↑↑ | Factor consumption |
| Fibrinogen | ↓↓ (<1.5 g/L) | Consumed — most sensitive marker. Normal in early DIC |
| D-dimer / FDPs | ↑↑↑ | Fibrinolysis product — markedly elevated |
| Blood film | Schistocytes | Microangiopathic haemolysis (distinguish from TTP) |
| Fibrinogen | ↓ (may be normal early) | Acute phase reactant — can mask fall initially |
Monitoring: Repeat ISTH DIC score, fibrinogen, PT, APTT, platelets every 4–6h in active DIC. Goal is to correct the coagulopathy while aggressively treating the underlying cause. Involve haematology, intensivist and relevant specialist early.
Thyroid Storm (Thyrotoxic Crisis)
Endocrine Society Guidelines · RCEM · Burch-Wartofsky Point Scale — Lugol's iodine, PTU, propranolol, steroids
Endocrine Society · RCEM 2024Thyroid storm carries 10–30% mortality even with treatment. Immediate multi-drug therapy is essential. Contact endocrinology, consider ITU. Do NOT wait for TFT results before starting treatment if clinical diagnosis is clear.
| Parameter | Finding | Points |
|---|---|---|
| Temperature (°C) | 37.2–37.7 | 5 |
| 37.8–38.3 | 10 | |
| 38.4–38.8 | 15 | |
| ≥38.9 | 20–30 | |
| Heart Rate (bpm) | 100–109 | 5 |
| 110–119 | 10 | |
| ≥120 | 15–25 | |
| AF | Present | 10 |
| CNS Effects | Mild agitation | 10 |
| Delirium/psychosis | 20 | |
| Seizure/coma | 30 | |
| Heart Failure | Mild (pedal oedema) | 5 |
| Severe (pulmonary oedema) | 25 | |
| GI/Hepatic | N/V/D, abdo pain | 10 |
| Jaundice | 20 | |
| Precipitant | Identified | 0 |
| Not identified | 10 |
Critical sequencing: give thionamide (PTU/carbimazole) FIRST, wait 1 hour, THEN give Lugol's iodine. Iodine given before thionamide will worsen thyroid storm (Jod-Basedow effect).
Plasmapheresis / plasma exchange — reserved for life-threatening thyroid storm refractory to all medical therapy. Discuss with endocrinology and HDU/ITU team. Rapidly removes circulating thyroid hormones.
Myxoedema Coma
Endocrine Society Guidelines · RCEM — T3/T4 IV replacement, hydrocortisone, rewarming, ventilatory support
Endocrine Society · RCEM 2024Myxoedema coma = life-threatening severe hypothyroidism with altered consciousness. Mortality 30–60% even with treatment. IV thyroid hormone replacement is essential — do not delay for TFT results. Contact endocrinology immediately.
Classic Features
Hypothermia (core temp often <35°C), altered consciousness/coma, bradycardia, hypotension, hypoventilation, macroglossia, dry skin, periorbital/peripheral oedema
Metabolic Derangements
Hyponatraemia (SIADH), hypoglycaemia, hypercapnia (type 2 respiratory failure), elevated CK, anaemia, pericardial/pleural effusions
Precipitants
Infection (most common), cold exposure, drugs (sedatives, opioids, anaesthesia, amiodarone, lithium), surgery, trauma, non-compliance with levothyroxine
History
Known hypothyroidism (ask family), thyroidectomy scar, radioiodine history, midline neck scar. Often elderly women
Pericardial effusion is common in myxoedema coma — USS heart to assess. Rarely causes tamponade; treat underlying hypothyroidism and monitor. Pericardiocentesis only if haemodynamic compromise.
Hyperosmolar Hyperglycaemic State (HHS)
JBDS-IP HHS Guidelines 2023 · RCEM — fluid strategy, osmolality monitoring, LMWH, insulin timing
JBDS 2023 · RCEMHHS carries 5–20% mortality — higher than DKA. Extreme hyperglycaemia (≥30 mmol/L), hyperosmolality ≥320 mOsm/kg, severe dehydration. Fluid replacement is the cornerstone. Do NOT rush insulin — wait until glucose not falling with fluids alone.
| Feature | HHS | DKA |
|---|---|---|
| Glucose | ≥30 mmol/L | ≥11 mmol/L (or known T1DM) |
| Osmolality | ≥320 mOsm/kg | Variable (often normal) |
| Ketones | <3 mmol/L blood / <2+ urine | ≥3 mmol/L blood / 2+ urine |
| Bicarbonate | >15 mmol/L | <15 mmol/L |
| pH | >7.3 | <7.3 |
| Onset | Days–weeks (insidious) | Hours–days |
| Fluid deficit | 8–10+ litres | 3–5 litres |
| Typical patient | Elderly T2DM | T1DM (any age) |
Mixed HHS/DKA (blood ketones ≥1 mmol/L + osmolality ≥320): treat with HHS fluid protocol + FRII at 0.05 units/kg/h from the start. Follow both glucose and osmolality targets.
Phaeochromocytoma / Paraganglioma Crisis
Endocrine Society Guidelines 2014 · RCEM · ESE 2020 — phentolamine, phenoxybenzamine, alpha-blockade first
Endocrine Society · ESE 2020NEVER give beta-blockers before alpha-blockade — causes unopposed alpha-adrenergic vasoconstriction → hypertensive crisis, organ failure, death. Alpha-blocker ALWAYS first.
Phaeochromocytoma in pregnancy: alpha-blockade (phenoxybenzamine) throughout pregnancy; delivery by caesarean section with simultaneous tumour resection at ≥24 weeks. High maternal and fetal mortality if unrecognised.
Beta-blocker / Calcium Channel Blocker Overdose
TOXBASE · RCEM Toxicology Guidelines · High-dose insulin, lipid emulsion, glucagon, ECMO
TOXBASE · RCEM 2024BB/CCB overdose can cause profound bradycardia, heart block, and cardiogenic shock refractory to conventional vasopressors. Call TOXBASE (0344 892 0111) early. Consider ECMO in refractory cases — do not delay referral.
| Feature | Beta-blocker OD | CCB OD |
|---|---|---|
| HR | Bradycardia | Bradycardia (non-dihydropyridine: verapamil/diltiazem) |
| BP | Hypotension | Profound hypotension |
| Glucose | Hypoglycaemia | Hyperglycaemia (blocks pancreatic insulin release) |
| Conduction | AV block, wide QRS (propranolol — Na channel) | AV block (verapamil/diltiazem), normal QRS |
| Consciousness | Seizures (propranolol CNS penetration) | Often preserved until late |
Tricyclic Antidepressant (TCA) Overdose
TOXBASE · RCEM · Sodium bicarbonate · QRS widening · Arrhythmia · Seizures
TOXBASE · RCEM 2024TCA OD can deteriorate rapidly — patients can arrest within minutes. QRS >100ms or right axis deviation = treat with sodium bicarbonate immediately. Secure airway early.
Opioid Toxidrome
TOXBASE · RCEM · NICE NG115 — Naloxone protocol, modified-release opioids, titration
TOXBASE · RCEM 2024Opioid toxidrome: miosis + CNS depression + respiratory depression. Naloxone half-life (60–90 min) is shorter than most opioids — re-narcotisation is common. Modified-release opioids require prolonged monitoring (12–24h) and naloxone infusion.
Organophosphate / Nerve Agent Poisoning
TOXBASE · RCEM · PHE CBRN Guidelines — Atropine, pralidoxime, PPE, decontamination
TOXBASE · PHE CBRN · RCEMDo NOT approach patient without PPE — skin/vapour exposure hazardous to rescuers. Decontamination before treatment. Atropine in massive doses may be required. Call TOXBASE (0344 892 0111) and PHE for nerve agent exposure.
Serotonin Syndrome
TOXBASE · RCEM — Hunter criteria, cyproheptadine, benzodiazepines, cooling, differentiate from NMS
TOXBASE · RCEM 2024Serotonin syndrome vs NMS: serotonin = rapid onset (hours), hyperreflexia + clonus (key), caused by serotonergic drugs. NMS = gradual onset (days), lead-pipe rigidity, dopamine antagonist. Treatment differs significantly.
NMS vs Serotonin Syndrome: NMS — slower onset, rigidity > clonus, caused by antipsychotics/dopamine antagonists, treat with dantrolene 1–2.5 mg/kg IV and bromocriptine. Cyproheptadine is NOT effective for NMS.
Carbon Monoxide Poisoning
TOXBASE · RCEM · UHMS — 100% O₂, COHb levels, hyperbaric oxygen criteria, pregnancy
TOXBASE · RCEM · UHMS 2024CO is odourless and colourless. SpO₂ pulse oximetry is UNRELIABLE — falsely normal. Diagnose with co-oximetry (ABG). All patients: 100% O₂ via tight-fitting non-rebreathe mask immediately. Remove from source.
| COHb (%) | Symptoms |
|---|---|
| 10–20% | Headache, nausea, fatigue — often misdiagnosed as viral illness |
| 20–40% | Severe headache, dizziness, confusion, tachycardia, dyspnoea |
| 40–60% | Altered consciousness, syncope, chest pain, arrhythmias |
| >60% | Coma, seizures, cardiovascular collapse, death |
Lithium Toxicity
TOXBASE · RCEM — Acute vs chronic toxicity, whole bowel irrigation, haemodialysis criteria
TOXBASE · RCEM 2024| Feature | Acute | Chronic |
|---|---|---|
| Who | Intentional OD, naive patient | Long-term user, therapeutic range exceeded |
| Serum level | Very high (>4 mmol/L) but less toxic | Moderate (1.5–2.5 mmol/L) but more toxic — tissue-loaded |
| Symptoms | GI prominent (N&V, diarrhoea) | Neurological prominent (tremor, ataxia, confusion, seizures) |
| Precipitants | OD | Dehydration, NSAIDs, ACEi/ARBs, infection, renal impairment, thiazides |
| Dialysis threshold | Level >5 mmol/L or severe symptoms | Level >2.5 mmol/L with severe neuro symptoms |
Digoxin Toxicity
TOXBASE · RCEM · BNF — DigiFab, ECG changes, magnesium, avoid DC cardioversion
TOXBASE · RCEM 2024Do NOT DC cardiovert in digoxin toxicity — can precipitate refractory VF. DigiFab is the definitive antidote. Contact cardiology and TOXBASE early.
Salicylate (Aspirin) Overdose
TOXBASE · RCEM — urinary alkalinisation, haemodialysis criteria, Done nomogram
TOXBASE · RCEM 2024Ethylene Glycol / Methanol Poisoning
TOXBASE · RCEM · EXTRIP Workgroup — Fomepizole, osmolar gap, haemodialysis, folinic acid
TOXBASE · EXTRIP · RCEMBoth are medical emergencies with significant mortality. Call TOXBASE immediately (0344 892 0111). Fomepizole (4-MP) is the antidote of choice — start before waiting for levels. Haemodialysis is definitive treatment.
| Feature | Ethylene Glycol | Methanol |
|---|---|---|
| Source | Antifreeze, de-icing fluid | Methylated spirits, brake fluid, bootleg alcohol |
| Toxic metabolite | Oxalic acid → calcium oxalate | Formic acid → formate |
| Target organ | Kidneys (AKI, oxalate crystals in urine) | Eyes (optic neuropathy → blindness), CNS |
| Early features | Inebriation (without alcohol smell), CNS depression | Inebriation, visual blurring, "snow-field" vision |
| Late features | Oliguric AKI, flank pain, hypocalcaemia, cardiac arrhythmias | Blindness, severe metabolic acidosis, coma, death |
| Urine findings | Calcium oxalate crystals | Normal |
| Latency to toxicity | 12–24h (during metabolism) | 12–24h (during metabolism) |
Ectopic Pregnancy
NICE NG126 (2019) · RCOG GTG No.21 · RCEM — β-hCG, USS, methotrexate, salpingectomy
NICE NG126 · RCOG GTG21Ruptured ectopic = haemorrhagic shock emergency. Any woman of reproductive age with abdominal pain + haemodynamic instability — suspect ectopic. Resuscitate and activate massive haemorrhage protocol. Emergency surgery without delay.
Postpartum Haemorrhage (PPH)
RCOG GTG No.52 (2016, updated 2023) · RCEM — Oxytocin, ergometrine, TXA, balloon tamponade, B-Lynch
RCOG GTG52 · 2023Primary PPH = ≥500 mL blood loss within 24h of delivery (major PPH ≥1000 mL). Call for help immediately — senior obstetrician, anaesthetist, midwife coordinator, haematologist. Activate MHP early. "4 Ts" cause: Tone (80%), Trauma, Tissue, Thrombin.
Pre-eclampsia
NICE NG133 (2023) · RCOG GTG No.10a — antihypertensives, MgSO₄ prophylaxis, delivery timing
NICE NG133 · RCOG 2023Eclampsia
RCOG GTG No.10a (2023) · NICE NG133 — MgSO₄ 4 g IV, airway, delivery, calcium gluconate antidote
RCOG GTG10a · 2023Eclampsia = seizure in pre-eclamptic patient. MgSO₄ is the treatment of choice — NOT diazepam or phenytoin for first-line. Call obstetric emergency team. Delivery is definitive treatment after stabilisation.
HELLP Syndrome
RCOG · ACOG — Haemolysis, Elevated Liver enzymes, Low Platelets · Delivery, steroids, supportive
RCOG · ACOG 2024HELLP = haemolysis + elevated liver enzymes + low platelets. Variant of severe pre-eclampsia. Maternal mortality 1–3%. Delivery is definitive treatment. Hepatic rupture/subcapsular haematoma = surgical emergency.
Intrahepatic Cholestasis of Pregnancy (ICP)
NICE NG207 (2021) · RCOG GTG No.43 — ursodeoxycholic acid, bile acids, fetal monitoring, delivery timing
NICE NG207 · RCOG GTG43Acute Fatty Liver of Pregnancy (AFLP)
RCOG · NICE — Third trimester emergency, ITU, delivery, NAC, liver failure management
RCOG · EASL 2023AFLP = rare but life-threatening liver failure in third trimester. Maternal mortality 1–18%. Delivery is the only definitive treatment. Admit to HDU/ITU immediately. Involves hepatology, obstetrics, neonatology, intensivist.
Endometritis / Puerperal Sepsis
RCOG GTG No.64a (2012, updated 2020) · NICE NG51 — antibiotics, Sepsis-6, source control
RCOG GTG64a · NICE NG51Group A Streptococcus (GAS) sepsis can be rapidly fatal in postpartum women — deterioration within hours. Think sepsis in any unwell postpartum woman. Apply Sepsis-6 within 1 hour. MBRRACE reports GAS as leading direct cause of maternal death.
Miscarriage & Early Pregnancy Complications
NICE NG126 (2019) · RCOG · RCEM — Types, management, anti-D, misoprostol, surgical options
NICE NG126 · RCOG 2023| Type | USS Findings | Clinical |
|---|---|---|
| Threatened | IUP visible, fetal heart present | PV bleeding, cervix closed. Viable pregnancy |
| Inevitable | Products in uterus/cervix | PV bleeding, cervix open, passage imminent |
| Incomplete | Retained products (heterogeneous mass) | Ongoing bleeding, some tissue passed. Cervix open |
| Complete | Empty uterus (<15 mm AP diameter) | All products passed, pain/bleeding settling |
| Missed | No fetal heartbeat: CRL ≥7 mm OR MSD ≥25 mm with no embryo | Often asymptomatic — incidental USS finding |
| Septic | Retained products ± gas in uterus | Fever, offensive discharge, uterine tenderness — emergency |
Shoulder Dystocia
RCOG GTG No.42 (2023) · RCEM — HELPERR mnemonic, McRoberts, suprapubic pressure, internal manoeuvres
RCOG GTG42 · 2023Shoulder dystocia = delivery of the head but failure of shoulder delivery with routine traction. Fetal hypoxia rapidly progressive — brain injury within 5 min. Call for help IMMEDIATELY. NEVER apply fundal pressure. NEVER pull on head laterally or rotate the neck.
Stevens-Johnson Syndrome / TEN
BAD / NICE guidelines · SCORTEN scoring · Dermatology emergency
BAD 2023 · RCEMLife-threatening mucocutaneous emergency. IMMEDIATELY stop all suspected causative drugs. Refer to burns/dermatology/ITU. Do NOT give corticosteroids.
SJS
Epidermal detachment <10% BSA. Mucosal involvement in 2+ sites. Atypical target lesions.
SJS/TEN Overlap
Epidermal detachment 10–30% BSA. High risk, urgent burns unit.
TEN
Epidermal detachment >30% BSA. Nikolsky sign +ve. Mortality up to 30–50%.
- 1Withdraw causative drug immediately. Every day of continued exposure increases mortality.
- 2Airway: early anaesthetic review — mucosal sloughing may compromise airway. Low threshold for intubation.
- 3IV access — avoid IM injections. Insert urinary catheter. Nasogastric tube for nutrition.
- 4IV fluid resuscitation — use Parkland formula: 3–4 mL/kg/% BSA involved over 24h (dextrose-saline or Ringer's lactate).
- 5Wound care: non-adhesive dressings (e.g. Mepitel). Do NOT debride intact blisters. Cool compresses for comfort.
- 6Ophthalmology urgent review — ocular involvement causes corneal scarring.
- 7Analgesia: regular paracetamol, opioids if needed. Avoid NSAIDs.
- 8Transfer to regional burns unit (preferably) or ITU if SCORTEN ≥3.
Angio-oedema
BSACI / RCEM guidelines · Allergic vs hereditary · Airway emergency
BSACI 2024 · RCEMLaryngeal/pharyngeal involvement = immediate airway emergency. Call anaesthetics. Prepare for surgical airway. Angioedema can progress rapidly to asphyxiation.
Allergic / Mast Cell (IgE-mediated)
Urticaria present. Rapid onset. Responds to adrenaline. Associated with anaphylaxis. Trigger: food, drugs, venom.
ACE Inhibitor-Induced
No urticaria. May occur months–years into treatment. Bradykinin mediated. Does NOT respond to adrenaline. Stop ACEi permanently.
Hereditary Angioedema (HAE)
C1-inhibitor deficiency (type 1) or dysfunction (type 2). Family history. Recurrent, unpredictable. NO urticaria. Bradykinin mediated.
Acquired Angioedema
C1-INH deficiency secondary to lymphoproliferative disease, autoimmune, or ACEI. Check C3, C4, C1q levels.
Necrotising Fasciitis
RCEM / BSAC guidelines · LRINEC score · Surgical emergency · IV antibiotics
RCEM · BSAC 2023Surgical emergency. Any delay to theatre increases mortality. "Finger test" (loss of resistance to blunt dissection) = immediate surgical debridement. Do NOT wait for imaging if diagnosis suspected.
Mortality of NF with surgery is ~20–25%; without surgery approaches 100%. The only life-saving intervention is wide radical surgical debridement — all necrotic tissue removed, repeat debridement in 24–48h.
Ludwig's Angina
Bilateral submandibular space infection · Airway emergency · Surgical drainage
RCEM · BAOMSLife-threatening infection of the floor of mouth. Airway compromise is the #1 killer. Early anaesthetic/ENT review is mandatory. Awake fibreoptic intubation preferred — anatomically distorted airway.
Epiglottitis
Supraglottitis · Adult & paediatric · Airway emergency · Haemophilus influenzae
RCEM · ENT UKDo NOT attempt oral examination or lateral neck X-ray in a child with stridor and drooling — may precipitate complete obstruction. Keep patient upright. Call ENT/anaesthetics immediately.
Epistaxis
BSACI / ENT UK guidelines · Anterior vs posterior · Cautery · Packing · Haemostasis
ENT UK 2021 · BSACIPosterior epistaxis can cause life-threatening haemorrhage. Elderly patients on anticoagulants are highest risk. Airway may be compromised by blood ingestion/aspiration.
- 1Patient upright, leaning forward. Pinch soft part of nose (not bony bridge) for 15 minutes continuous — do NOT release early.
- 2Spit out blood (do not swallow — causes nausea/vomiting). Ice pack to back of neck optional.
- 3Assess: BP, HR, haematological history. IV access if heavy bleed. Blood group & save or crossmatch if unstable.
- 4Examine nasal cavity with Thudichum speculum and light — identify anterior (Little's area — Kiesselbach's plexus) vs posterior source.
- 5Topical anaesthetic + vasoconstrictor: Co-phenylcaine (lidocaine + phenylephrine) spray — 2 sprays per nostril, wait 3 minutes.
Acute Psychosis & Behavioural Emergency
NICE NG10 · NICE NG185 · Rapid tranquillisation · Mental Capacity Act
NICE NG10 2015 · RCEM 2024Always exclude organic cause first (hypoglycaemia, sepsis, metabolic, neurological, substance intoxication). Mental Health Act assessment if patient lacks capacity and poses risk. De-escalation first; medications second.
Delirium & Dementia Emergencies
NICE NG97 · 4AT screening · Non-pharmacological · Reversible causes
NICE NG97 2019 · RCEMDelirium is always organic until proven otherwise. 30-40% of hospitalised elderly develop delirium. Associated with 3x mortality. Non-pharmacological measures are first-line. Treat the underlying cause.
Hyperactive Delirium
Agitation, combativeness, hallucinations (usually visual). More often recognised. Risk of injury.
Hypoactive Delirium
Quieter, withdrawn, reduced consciousness. Often MISSED. Worse prognosis. Common post-op/critically ill.
Mixed Delirium
Fluctuates between hyperactive and hypoactive. Most common form. Disruptive at times, withdrawn at others.
NMS & Serotonin Syndrome
Neuroleptic malignant syndrome vs serotonin syndrome · Hunter criteria · Dantrolene · Cooling
RCEM · TOXBASE 2024Both are life-threatening drug reactions with hyperthermia. Distinguish: NMS = slow onset (days), rigidity prominent, caused by antipsychotics. Serotonin syndrome = rapid onset (hours), clonus/hyperreflexia prominent, caused by serotonergic drugs.
NMS
Onset: days–weeks. Cause: antipsychotics (haloperidol, clozapine). Rigidity: "lead-pipe" severe. Tremor: less prominent. Clonus: absent/mild. Pupils: normal. Reflexes: reduced/normal.
Serotonin Syndrome
Onset: hours. Cause: SSRIs, SNRIs, MAOIs, tramadol, linezolid, triptans, fentanyl. Rigidity: less severe. Clonus: prominent (diagnostic). Pupils: mydriasis. Hyperreflexia. Agitation/tremor.
Lithium Toxicity
Acute vs chronic toxicity · TOXBASE · Haemodialysis indications · Monitoring
TOXBASE · RCEM 2024Therapeutic range 0.6–1.0 mmol/L. Toxicity usually >1.5 mmol/L (chronic) or >2.0 mmol/L (acute). Chronic toxicity more dangerous at lower levels. Always check renal function.
Mild (Li 1.5–2.0)
Nausea, vomiting, diarrhoea, tremor, polyuria, thirst. Usually manageable with hydration.
Moderate (Li 2.0–2.5)
Confusion, drowsiness, coarse tremor, muscle twitching, slurred speech, ataxia.
Severe (Li >2.5)
Seizures, coma, cardiovascular instability, respiratory failure. Haemodialysis likely required.
Major Trauma Primary Survey
ATLS 10th Ed · cABCDE · Damage control resuscitation · Massive haemorrhage protocol
ATLS 10th Ed · RCSUK · NICE NG39Pre-alert trauma team. CABCDE approach. Control catastrophic haemorrhage FIRST. Permissive hypotension (SBP 80–90 mmHg) until surgical control achieved. Activate massive haemorrhage protocol early.
Trauma Secondary Survey
ATLS · Head-to-toe examination · AMPLE history · Adjuncts & imaging
ATLS 10th Ed · RCSUKOnly commence secondary survey once primary survey complete, life-threatening injuries managed, and patient haemodynamically stable. The secondary survey is a complete head-to-toe physical examination.
Paediatric Trauma & Advanced Life Support
APLS · WETFLAG · Paediatric trauma · IO access · Weight estimation
APLS · RCUK 2021 · RCSUKChildren are not small adults. Physiological compensation masks shock until late decompensation. Tachycardia is the earliest sign of shock. Use WETFLAG or Broselow tape for weight-based dosing. Normal HR/BP varies by age.
Emergency Department Thoracotomy
EDT indications · Left anterolateral approach · Resuscitative thoracotomy · Cardiac massage
RCSUK · RCEM · EAST GuidelinesLast-resort procedure. Survival depends on mechanism and arrest duration. Penetrating trauma has much better outcomes (up to 35% survival) vs blunt trauma (<2%). Do NOT perform without senior surgical/trauma presence.
Burns Emergency Management
Parkland formula · Wallace Rule of Nines · Airway burns · Carbon monoxide · Cyanide
NBCN Guidelines · NICE · RCEMAirway assessment is priority — inhalation injury is the #1 killer in burns. Remove from exposure. Cool with cool running water 15–20°C for 20 minutes (not ice). Cling film dressings. Early referral to burns centre.
Superficial (Epidermal)
Erythema, painful, NO blisters. Heals 7–10 days spontaneously. Not included in TBSA calculation.
Superficial Partial-Thickness
Blisters, moist, pink, very painful. Heals 14–21 days. Include in TBSA.
Deep Partial-Thickness
Pale/mottled, reduced sensation, blistered. Requires grafting. Include in TBSA.
Full-Thickness
Leathery/charred, painless, waxy. Always requires grafting. Include in TBSA.
Spinal Cord Injury
ASIA grading · Spinal cord syndromes · Neurogenic shock · Steroid controversy
RCSUK · NICE NG41 · ISNCSCISpinal precautions until injury excluded. SBP target ≥90 mmHg (avoids secondary cord ischaemia). Avoid hypoxia. Neurogenic shock (bradycardia + hypotension) requires vasopressors, NOT fluids alone.
Spinal & Facial Fractures
Cervical fracture patterns · Le Fort · Mandibular · Odontoid · Hangman · Jefferson
RCSUK · NICE · BAOMSAll high-energy cervical spine fractures: maintain immobilisation until cleared. CT is investigation of choice (plain films miss up to 15% of fractures). Neurosurgical/spinal surgery referral for unstable fractures.
Crush Injury & Compartment Syndrome
Rhabdomyolysis · Fasciotomy · 6 Ps · Compartment pressure measurement
RCSUK · NICE · BOA 2023Compartment syndrome: clinical diagnosis. Do NOT wait for compartment pressure measurement if classic signs present. Fasciotomy within 6 hours prevents irreversible muscle necrosis. Pain out of proportion and pain with passive stretch are earliest signs.