Emergency Medicine

Key Facts

ALS provides a systematic framework for managing cardiac arrest using a team-based approach. It builds on basic life support (BLS) by adding defibrillation, drug therapy, advanced airway management, and systematic identification and treatment of reversible causes.

Epidemiology

ALS-trained healthcare professionals manage approximately 50,000 cardiac arrests per year in the UK (combined OHCA and IHCA). ALS training is mandatory for most hospital doctors in the UK. Successful resuscitation depends on the entire chain of survival, not any single intervention.

Aetiology

Cardiac arrest may result from primary cardiac causes (acute coronary syndromes, arrhythmias, structural heart disease) or non-cardiac causes (respiratory failure, sepsis, haemorrhage, PE, metabolic derangement, toxins). The approach is the same regardless of cause, with specific attention to identifying and treating reversible factors.

Pathophysiology

The ALS algorithm is based on the principle that early defibrillation is the only intervention proven to improve survival from VF/pVT, while for non-shockable rhythms, treating the underlying cause is paramount. Adrenaline increases coronary and cerebral perfusion pressure during CPR. Amiodarone stabilises the myocardial membrane in refractory VF.

ALS Assessment

• Confirm cardiac arrest: Unresponsive, not breathing normally, no pulse
• Attach defibrillator: Assess rhythm - shockable vs non-shockable
• Begin CPR: 30:2 initially; continuous once advanced airway placed

Shockable Rhythm Protocol

1. Single defibrillation (150-200J biphasic)
2. Immediately resume CPR for 2 minutes
3. Rhythm check - shock again if VF/pVT persists
4. After 3rd shock: Adrenaline 1mg IV + Amiodarone 300mg IV
5. Continue cycle; Adrenaline every 3-5 min; Amiodarone 150mg after 5th shock

Non-Shockable Rhythm Protocol

1. Begin CPR, secure IV access
2. Adrenaline 1mg IV as soon as possible
3. Continue CPR for 2 minutes, then rhythm check
4. Adrenaline every 3-5 min
5. Actively search for and treat reversible causes

Red Flags

• CPR interrupted for >10 seconds - no-flow time increases brain injury
• Failure to recognise PEA with treatable cause - delays definitive treatment
• Team not considering 4Hs/4Ts - missed reversible causes
• Post-ROSC hypoxia and hypotension - worsen neurological outcome

Bedside

• Cardiac rhythm monitoring: Continuous - guide shockable vs non-shockable pathway
• Capnography (ETCO2): Confirms ETT placement; guides CPR quality (target ETCO2 >2.7 kPa); sudden rise = ROSC
• Point-of-care USS: During rhythm check (<10 sec) - cardiac standstill, tamponade, RV dilatation
• Blood gas (ABG/VBG): K⁺, pH, lactate during arrest

Bloods

• ABG: Immediate - potassium, pH, lactate, haemoglobin
• Blood glucose: Hypoglycaemia is a treatable cause
• U&Es: Post-ROSC renal function and electrolytes
• Troponin: Post-ROSC cardiac assessment

Imaging

• 12-lead ECG: Post-ROSC - STEMI diagnosis
• CXR: Post-ROSC - ETT position, complications
• CT: If cause of arrest unclear (head, chest, abdomen)

Special Tests

• Echocardiography: Post-ROSC cardiac function assessment
• Coronary angiography: If ACS suspected
• CT head and EEG: For neuroprognostication (≥72h post-arrest)

Non-pharmacological

• Team leadership: Designated team leader; clear role allocation
• High-quality CPR: Continuous compressions (100-120/min, 5-6cm), rotate compressors every 2 min
• Defibrillation: Biphasic 150-200J; minimise pre-shock pause (<5 sec)
• Advanced airway: ETT or SGA; once placed, continuous compressions (10 ventilations/min)
• IV/IO access: Peripheral IV preferred; IO if IV access fails within 2 min

Pharmacological

• Adrenaline 1mg IV: Non-shockable - immediately; Shockable - after 3rd shock; then every 3-5 min
• Amiodarone 300mg IV: After 3rd shock; 150mg after 5th shock
• Lidocaine 1mg/kg IV: Alternative to amiodarone if unavailable
• Sodium bicarbonate 50mmol (50mL of 8.4%): Consider for severe acidosis, hyperkalaemia, or TCA overdose
• Calcium chloride 10mL 10% IV: For hyperkalaemia, hypocalcaemia, or calcium channel blocker overdose
• Magnesium 2g (8mmol) IV: For torsades de pointes or hypomagnesaemia
• Thrombolysis (alteplase 50mg IV): For suspected massive PE - continue CPR for 60-90 min after

Surgical/Interventional

• Emergency thoracotomy: Penetrating chest trauma with arrest
• Pericardiocentesis: Cardiac tamponade
• Needle decompression → chest drain: Tension pneumothorax
• ECPR (extracorporeal CPR): For refractory cardiac arrest in selected patients

Referral Criteria

• All ROSC patients - ICU for post-resuscitation care
• STEMI post-ROSC - emergency PCI
• Refractory VF - consider ECPR if available
• Survivors - cardiac assessment and ICD consideration

• OHCA VF survival: ~25-30% with bystander CPR and early defibrillation
• OHCA PEA/asystole survival: <5%
• IHCA overall survival to discharge: ~23-25%
• Duration of CPR: Survival decreases with duration but ROSC has been reported after >60 min in hypothermic or toxicological arrests
• Neurological outcome: ~80% of survivors achieve CPC 1-2 (good/moderate outcome)
• Targeted temperature management: TTM2 trial showed no benefit of 33°C over 36°C, but both better than uncontrolled hyperthermia

4Hs and 4Ts - Reversible Causes

ALS Drug Summary

Key Facts

Anaphylaxis is a medical emergency requiring immediate recognition and treatment with adrenaline. It is an IgE-mediated (or non-IgE mediated) systemic allergic reaction that can be fatal within minutes. All healthcare professionals should be able to recognise and treat anaphylaxis.

Epidemiology

Anaphylaxis incidence is approximately 50-100 per 100,000 person-years in the UK and is increasing, particularly food-triggered reactions. Fatal anaphylaxis accounts for approximately 20 deaths per year in the UK. Food is the most common trigger in children; drugs and insect stings in adults.

Aetiology

• Food: Peanuts, tree nuts, shellfish, milk, eggs, sesame, wheat (most common trigger in children)
• Drugs: Antibiotics (penicillin), NSAIDs, anaesthetic agents
• Insect venom: Bee and wasp stings
• Latex: Healthcare workers, patients with spina bifida
• Exercise-induced: Particularly food-dependent exercise-induced anaphylaxis
• Idiopathic: No trigger identified in ~20%

Pathophysiology

Anaphylaxis is primarily a type I (IgE-mediated) hypersensitivity reaction. Cross-linking of IgE on mast cells and basophils triggers degranulation and release of histamine, tryptase, leukotrienes, and prostaglandins. This causes vasodilation (hypotension), increased vascular permeability (oedema, urticaria), bronchospasm, and upper airway oedema. Non-IgE-mediated (anaphylactoid) reactions produce identical clinical features via direct mast cell activation.

Diagnostic Criteria (Any ONE of the following with acute onset)

• Airway: Swelling of tongue, throat, laryngeal oedema, stridor, hoarseness
• Breathing: Bronchospasm, wheeze, increased work of breathing, cyanosis, SpO2 <92%
• Circulation: Hypotension, tachycardia, pale, clammy, reduced consciousness, cardiac arrest
• Skin/mucosal: Urticaria, erythema, angioedema (present in ~80% but may be absent)
• GI: Abdominal pain, vomiting, diarrhoea

Rapid Onset (Usually Within Minutes)

• Skin changes may precede or follow systemic features
• Cardiovascular collapse may be the ONLY feature (especially drug-triggered)
• GI symptoms common in food-triggered anaphylaxis

Red Flags

• Stridor or tongue swelling - imminent airway obstruction
• Wheeze with desaturation - severe bronchospasm
• Hypotension unresponsive to initial adrenaline - repeat dose at 5-min intervals
• Previous fatal/near-fatal anaphylaxis - high-risk patient
• Asthma - increases severity of anaphylaxis (respiratory arrest risk)

Bedside

• Clinical diagnosis: Do NOT delay treatment for investigations
• Observations: SpO2, BP, HR - continuous monitoring
• Peak flow: If bronchospasm predominant

Bloods

• Serum tryptase: Sample 1 - as soon as feasible after treatment; Sample 2 - 1-2 hours; Sample 3 - >24 hours (baseline). Elevated tryptase confirms mast cell degranulation. May be normal in food-triggered anaphylaxis.
• ABG: If respiratory compromise

Imaging

• CXR: If respiratory distress - exclude pneumothorax, aspiration

Special Tests

• Specialist allergy testing (6 weeks post-event): Skin prick tests, specific IgE for suspected triggers, component-resolved diagnostics
• Serum IgE and specific IgE: To suspected allergens
• Drug provocation testing: In selected cases with specialist supervision

Non-pharmacological

• Remove trigger: Stop drug infusion, remove insect sting (scrape, don't squeeze)
• Position: Supine with legs raised (if breathing allows); seated if respiratory distress predominant
• Call for help: 999 or 2222
• High-flow oxygen: 15L/min via non-rebreather mask

Pharmacological

• Adrenaline IM (1:1000): Adult 500mcg (0.5mL); Child 6-12yr 300mcg; Child <6yr 150mcg - anterolateral thigh. Repeat every 5 min if no improvement.
• IV fluids: 500mL-1L crystalloid bolus (20mL/kg in children) - repeat as needed for hypotension
• Chlorphenamine IV: Adult 10mg; Child 6-12yr 5mg; <6yr 2.5mg
• Hydrocortisone IV: Adult 200mg; Child 6-12yr 100mg; <6yr 50mg (prevents biphasic reaction)
• Bronchospasm: Salbutamol 5mg nebulised; ipratropium 500mcg nebulised
• Refractory anaphylaxis: IV adrenaline 50mcg boluses (1mL of 1:10,000); adrenaline infusion 0.05-1mcg/kg/min; glucagon 1-2mg IV if on beta-blockers

Surgical/Interventional

• Emergency intubation/cricothyroidotomy: If complete airway obstruction from angioedema

Referral Criteria

• ALL patients with anaphylaxis - refer to specialist allergy clinic
• Prescribe 2 adrenaline auto-injectors (EpiPen/Jext) with training
• Provide personalised anaphylaxis action plan
• MedicAlert bracelet recommended
• If drug-triggered - report via Yellow Card Scheme

• Mortality: <1% overall; ~20 deaths/year in UK from anaphylaxis
• Food anaphylaxis: Most common cause of fatal anaphylaxis in young people
• Drug anaphylaxis: Most common cause of fatal anaphylaxis in adults
• Delayed adrenaline: Single most important factor in fatal anaphylaxis - every patient should carry 2 auto-injectors
• Biphasic reactions: 5-20% at 4-12 hours - all patients observed for minimum 6-12 hours
• Long-term: Excellent prognosis with allergen avoidance and emergency action plan; venom immunotherapy is 95% effective for insect sting allergy

Adrenaline Auto-Injector Doses

Resuscitation Council UK Anaphylaxis Algorithm (Simplified)

Key Facts

Severe allergic reactions are common presentations to emergency departments. The key clinical decision is whether the reaction constitutes anaphylaxis (requiring adrenaline) or a non-anaphylactic allergic reaction (managed with antihistamines and observation).

Epidemiology

Allergic disease affects approximately 30-40% of the UK population. ED attendances for allergic reactions have doubled over the past 20 years. Acute urticaria is the most common allergic presentation. Angioedema without anaphylaxis accounts for approximately 100,000 ED attendances annually.

Aetiology

• IgE-mediated (type I): Food, drugs, insect stings, latex - rapid onset (minutes to hours)
• Non-IgE mediated: ACEi-induced angioedema (bradykinin-mediated), contrast media reactions
• Hereditary angioedema: C1 esterase inhibitor deficiency - autosomal dominant
• Chronic spontaneous urticaria: Autoimmune (anti-IgE or anti-FcεRI antibodies) in many cases

Pathophysiology

Allergic reactions involve mast cell and basophil degranulation releasing histamine, leukotrienes, and prostaglandins. In non-anaphylactic reactions, these mediators cause localised effects (urticaria, angioedema) without systemic cardiovascular or respiratory compromise. HAE is mediated by excess bradykinin production due to C1 esterase inhibitor deficiency - this is NOT a histamine-mediated process.

Acute Urticaria

• Raised, itchy wheals (hives) on any body surface
• Each wheal lasts <24 hours, new ones may appear
• Resolves spontaneously or with antihistamines

Angioedema (Without Anaphylaxis)

• Deep swelling of eyelids, lips, tongue, hands, feet, genitalia
• Non-pitting, often asymmetric
• May affect larynx (stridor) - monitor closely
• ACEi-induced: Occurs in ~0.5% of users; may develop after years of use

Hereditary Angioedema

• Recurrent episodes of angioedema WITHOUT urticaria
• Family history (autosomal dominant)
• Often triggered by trauma, stress, infection, oestrogens
• Does NOT respond to antihistamines, steroids, or adrenaline

Red Flags

• Tongue/laryngeal swelling with voice change or stridor - imminent airway obstruction
• Any sign of ABC compromise - escalate to anaphylaxis protocol
• Recurrent angioedema without urticaria - consider HAE (check C4, C1 inhibitor)
• ACEi use with angioedema - stop ACEi permanently (can switch to ARB with caution)

Bedside

• Clinical assessment: Identify whether anaphylaxis criteria are met (ABC involvement)
• Observations: SpO2, BP, HR, RR - monitor for progression
• Airway assessment: Voice change, stridor, tongue protrusion

Bloods

• Serum tryptase: If anaphylaxis suspected (take at 1h and 24h)
• C4 level: Screening test for HAE - low C4 between and during attacks
• C1 esterase inhibitor level and function: Confirm HAE diagnosis
• Specific IgE / RAST: For suspected allergens (food, drug, venom)
• FBC: Eosinophilia may suggest allergic/parasitic cause

Imaging

• Not routinely required; lateral soft tissue neck X-ray if concern about laryngeal oedema

Special Tests

• Skin prick testing: Specialist allergy clinic - 6 weeks post-reaction
• Drug provocation testing: For drug allergy confirmation
• Autologous serum skin test: For chronic spontaneous urticaria (autoimmune)

Non-pharmacological

• Allergen avoidance: Identify and remove trigger
• Patient education: Provide written allergy action plan
• MedicAlert bracelet: For severe allergies
• Dietitian referral: If food allergy (ensure nutritional adequacy)

Pharmacological

Acute urticaria/angioedema (no ABC compromise):

• Cetirizine 10mg PO or chlorphenamine 10mg IV/IM (acute setting)
• Prednisolone 40mg PO for 3-5 days if severe or not responding
• Ranitidine 50mg IV (H2 blocker) - adjunct in severe urticaria

ACEi-induced angioedema:

• Stop ACEi permanently
• Supportive care; adrenaline/antihistamines have limited efficacy (bradykinin-mediated)
• If severe airway compromise - intubation or surgical airway
• Consider icatibant (bradykinin B2 receptor antagonist) if available

Hereditary angioedema:

• Acute attack: C1 esterase inhibitor concentrate (Berinert 20 IU/kg IV) or icatibant 30mg SC
• Prophylaxis: Danazol 200-600mg/day (androgenic side effects) or tranexamic acid 1-1.5g BD-TDS; lanadelumab SC (anti-kallikrein antibody)

Chronic urticaria (>6 weeks):

• Non-sedating antihistamine (cetirizine/loratadine) - up to 4× standard dose
• Add ranitidine or montelukast
• Omalizumab (anti-IgE) for refractory chronic spontaneous urticaria (NICE TA339)

Referral Criteria

• Suspected anaphylaxis - allergy clinic referral + auto-injector prescription
• Recurrent angioedema without urticaria - immunology (HAE workup)
• Chronic urticaria refractory to antihistamines - dermatology/allergy
• Drug allergy confirmation needed - specialist allergy service

• Acute urticaria: Self-limiting in most cases; resolves within days to weeks
• Chronic urticaria: 50% resolve within 1 year; some persist for years; omalizumab effective in ~70%
• ACEi angioedema: Resolves within 24-72 hours of stopping ACEi; rare fatalities from airway obstruction
• HAE: Lifelong condition; laryngeal attacks carry mortality risk; modern treatments have dramatically improved outcomes
• Drug allergy: Accurate documentation prevents re-exposure; most drug 'allergies' are intolerances not true IgE-mediated allergy

Distinguishing Anaphylaxis from Severe Allergic Reaction

Types of Angioedema

Key Facts

Acute asthma exacerbations are one of the most common medical emergencies in the UK. Deaths from asthma are largely preventable and are associated with underestimation of severity, inadequate treatment, and poor follow-up. BTS/SIGN guidelines provide a structured approach.

Epidemiology

Asthma affects approximately 5.4 million people in the UK. There are approximately 77,000 hospital admissions for asthma annually. Approximately 1,400 people die from asthma each year in the UK. The UK has one of the highest asthma mortality rates in Europe.

Aetiology

Acute exacerbations are triggered by:

• Viral infections (most common trigger, especially rhinovirus)
• Allergen exposure: Pollen, dust mite, animal dander
• Exercise, cold air, emotional stress
• Non-adherence to preventer inhalers (most common modifiable factor)
• Drugs: NSAIDs, beta-blockers, aspirin
• Occupational exposures

Pathophysiology

Acute asthma involves bronchospasm (smooth muscle contraction), airway inflammation (oedema, cellular infiltration), and mucus hypersecretion. This causes progressive airway obstruction, hyperinflation, and ventilation-perfusion mismatch. In severe cases, respiratory muscle fatigue leads to hypoventilation, CO2 retention, and respiratory arrest.

Severity Classification (BTS/SIGN)

Moderate acute asthma:

• Increasing symptoms, PEF 50-75% best/predicted
• No features of acute severe asthma

Acute severe asthma (any one of):

• PEF 33-50% best/predicted
• Respiratory rate ≥25/min
• Heart rate ≥110/min
• Inability to complete sentences in one breath

Life-threatening (any one of):

• PEF <33% best/predicted
• SpO2 <92% or PaO2 <8 kPa
• Normal or raised PaCO2 (>4.6 kPa) - indicates exhaustion
• Silent chest, cyanosis
• Poor respiratory effort, altered consciousness
• Hypotension, arrhythmia

Near-fatal:

• Raised PaCO2 requiring mechanical ventilation

Red Flags

• Normal/rising CO2 in acute asthma - indicates respiratory failure (NOT reassuring)
• Silent chest - severe bronchospasm with minimal air entry
• Altered consciousness - imminent respiratory arrest
• Previous ICU admission for asthma - high-risk patient

Bedside

• PEF: Essential - correlate with best/predicted; repeat after treatment
• SpO2: Continuous monitoring
• ABG/VBG: If SpO2 <92% or life-threatening features - assess PaCO2

Bloods

• ABG: If severe/life-threatening - PaCO2, PaO2, pH, lactate
• FBC: Neutrophilia (infection), eosinophilia (allergic component)
• U&Es: If IV aminophylline considered; K⁺ monitoring (salbutamol causes hypokalaemia)
• CRP: If infection suspected
• Theophylline level: If on maintenance theophylline before aminophylline loading

Imaging

• CXR: If first episode, diagnostic uncertainty, life-threatening features, failure to respond (exclude pneumothorax, infection, foreign body)

Special Tests

• Blood/sputum eosinophil count: Guide biologic therapy eligibility in recurrent exacerbators
• FeNO: When stable - assess eosinophilic airway inflammation

Non-pharmacological

• Position: Sit patient upright
• High-flow oxygen: 15L/min via non-rebreather to maintain SpO2 94-98%
• Reassess frequently: PEF, SpO2, clinical status at 15-30 min intervals

Pharmacological

Immediate treatment (all acute severe):

• Salbutamol 5mg nebulised (driven by O2 at 6-8 L/min) - repeat every 15-30 min or back-to-back if life-threatening
• Ipratropium bromide 500mcg nebulised - add for severe/life-threatening
• Prednisolone 40-50mg PO (or hydrocortisone 100mg IV if unable to swallow) - continue for at least 5 days

If life-threatening or poor response:

• IV magnesium sulphate 1.2-2g (50% solution) over 20 minutes - single dose
• IV aminophylline loading dose 5mg/kg over 20 min (NOT if on oral theophylline) - then maintenance 0.5-0.7mg/kg/hr
• IV salbutamol 250mcg slow IV bolus - if nebulisation ineffective

If near-fatal/failing treatment:

• ICU referral: Intubation and mechanical ventilation
• Ketamine: May be used as bronchodilator at induction
• Volatile anaesthetic agents: Sevoflurane/isoflurane provide bronchodilation

Surgical/Interventional

• Intubation and ventilation: Last resort - high risk of dynamic hyperinflation and cardiac arrest
• Chest drain: If pneumothorax complicates acute asthma

Referral Criteria

• Life-threatening features - immediate ICU referral
• Poor response to initial treatment (PEF not improving >15 min) - senior review
• Previous near-fatal asthma - low threshold for ICU
• All patients - GP follow-up within 48 hours; respiratory specialist review within 4 weeks of hospital admission

• Hospital mortality for acute asthma: <1% overall; higher in life-threatening/near-fatal
• Risk factors for fatal asthma: Previous ICU admission, ≥3 ED attendances/year, poor adherence to treatment, psychosocial factors, brittle asthma
• Post-discharge: 30% readmission rate within 12 months if no structured follow-up
• Structured discharge planning: Reduces readmission by 30-40%
• The UK has one of the highest asthma mortality rates in Europe - the National Review of Asthma Deaths (NRAD) found most deaths were preventable

BTS/SIGN Acute Asthma Treatment Ladder

Discharge Checklist (BTS/SIGN)

Key Facts

Acute exacerbations of COPD (AECOPD) are major events in the natural history of the disease, associated with accelerated lung function decline, reduced quality of life, and increased mortality. Prompt treatment and structured follow-up are essential.

Epidemiology

COPD is the 5th leading cause of death in the UK. There are approximately 115,000 emergency hospital admissions for AECOPD annually. In-hospital mortality is approximately 7-10%. The 90-day mortality after an exacerbation is approximately 15%. COPD costs the NHS approximately £1.9 billion annually.

Aetiology

• Infective (most common): Viral (rhinovirus, influenza, RSV) ~50%; bacterial (H. influenzae, S. pneumoniae, M. catarrhalis) ~30%; mixed ~20%
• Non-infective: Air pollution, cold weather, non-adherence, PE, pneumothorax, heart failure
• Frequent exacerbators: ≥2 exacerbations/year - distinct phenotype with worse outcomes

Pathophysiology

Exacerbations involve increased airway inflammation, bronchospasm, and mucus hypersecretion leading to worsened airflow obstruction, dynamic hyperinflation, and ventilation-perfusion mismatch. In severe cases, respiratory muscle fatigue leads to hypercapnic respiratory failure (type 2). Excessive supplemental oxygen suppresses hypoxic respiratory drive, worsening CO2 retention via the Haldane effect and V/Q redistribution.

Clinical Features

• Increased dyspnoea, increased sputum volume and/or purulence, increased cough
• Wheeze, tachypnoea, use of accessory muscles
• Peripheral oedema (cor pulmonale)
• Confusion, drowsiness (hypercapnia - CO2 narcosis)

Severity Assessment

• Mild: Increased breathlessness, can manage at home with increased bronchodilators
• Moderate: Requires steroid ± antibiotic course
• Severe: Hospital admission required - respiratory failure, failure of outpatient treatment

Red Flags

• Altered consciousness (confusion, drowsiness) - hypercapnic respiratory failure
• pH <7.35 with PaCO2 >6 kPa - respiratory acidosis requiring NIV
• SpO2 <88% on controlled O2 - severe exacerbation
• pH <7.25 despite NIV - consider intubation and ICU
• Acute onset pleuritic chest pain - consider PE or pneumothorax

Bedside

• ABG: Essential - pH, PaCO2, PaO2, lactate (guides need for NIV)
• SpO2: Target 88-92% on controlled O2
• Sputum sample: If purulent - MC&S
• ECG: Exclude MI, arrhythmia; may show P pulmonale, right axis deviation

Bloods

• FBC: WCC (infection), Hb (polycythaemia in chronic hypoxia)
• CRP: Infection marker
• U&Es: Renal function, K⁺
• BNP/NT-proBNP: If heart failure co-existing
• Theophylline level: If on maintenance theophylline
• Blood cultures: If fever/septic

Imaging

• CXR: Exclude pneumonia, pneumothorax, effusion, heart failure
• CTPA: If PE suspected (Wells score assessment)

Special Tests

• Sputum culture: Guide antibiotic therapy
• Spirometry: NOT during acute exacerbation - perform when stable to confirm diagnosis and severity

Non-pharmacological

• Controlled oxygen therapy: 24-28% Venturi mask to target SpO2 88-92%; titrate up cautiously; repeat ABG at 30-60 min
• Physiotherapy: Chest physiotherapy for sputum clearance
• Fluid balance: Avoid fluid overload

Pharmacological

• Nebulised bronchodilators: Salbutamol 5mg + ipratropium 500mcg QDS (drive with air if hypercapnic; supplement O2 via nasal prongs)
• Prednisolone 30mg PO for 5 days (REDUCE trial)
• Antibiotics (if increased sputum purulence): Amoxicillin 500mg TDS or doxycycline 200mg day 1 then 100mg OD for 5 days; co-amoxiclav 625mg TDS if severe
• IV aminophylline: 5mg/kg loading then 0.5mg/kg/hr if poor response (NOT if on oral theophylline)

NIV (Non-Invasive Ventilation)

• Indication: Respiratory acidosis pH 7.25-7.35 with PaCO2 >6 kPa despite optimal medical therapy
• Settings: BiPAP - IPAP 12-20 cmH2O, EPAP 4-6 cmH2O; titrate to response
• Repeat ABG: At 1-2 hours - if no improvement, escalate
• NIV reduces mortality by 46% and intubation rates (Cochrane review)

Surgical/Interventional

• Intubation and invasive ventilation: If NIV fails (pH <7.25 despite NIV), patient deteriorating, or not suitable for NIV
• Chest drain: If pneumothorax

Referral Criteria

• pH <7.35 with PaCO2 >6 kPa - NIV required (respiratory ward or HDU)
• pH <7.25 despite NIV or not suitable for NIV - ICU referral
• All admitted patients - pulmonary rehabilitation referral within 4 weeks of discharge
• Recurrent exacerbations - respiratory specialist review

• In-hospital mortality: ~7-10% for admitted exacerbations
• 90-day mortality post-exacerbation: ~15%
• 1-year mortality after severe exacerbation: ~25%
• Readmission: ~30% readmitted within 30 days
• NIV: Reduces in-hospital mortality from ~20% to ~10% in acidotic patients
• Pulmonary rehabilitation post-exacerbation: Reduces readmission by 50% and improves quality of life
• Each exacerbation accelerates FEV1 decline and worsens prognosis

NICE/BTS NIV Criteria for COPD Exacerbation

Discharge Bundle

Key Facts

Acute coronary syndromes result from acute myocardial ischaemia, usually due to coronary atherosclerotic plaque rupture with thrombosis. Rapid diagnosis and treatment save lives and preserve myocardium. The UK has well-established primary PCI networks.

Epidemiology

ACS affects approximately 100,000 people per year in England. STEMI accounts for approximately 30% and NSTEMI/UA for 70%. STEMI 30-day mortality has fallen to approximately 7% with primary PCI. NSTEMI 30-day mortality is approximately 5% but 1-year mortality may exceed STEMI due to older age and more comorbidities.

Aetiology

• Plaque rupture/erosion: Most common mechanism - exposes thrombogenic subendothelial matrix
• Risk factors: Smoking, hypertension, diabetes, dyslipidaemia, family history, obesity, age, male sex
• Type 2 MI: Myocardial oxygen supply-demand mismatch (sepsis, anaemia, tachyarrhythmia)
• Other causes: Coronary spasm (Prinzmetal's), coronary dissection (young women, pregnancy), cocaine

Pathophysiology

Typical ACS Presentation

• Central chest pain/tightness/heaviness - may radiate to left arm, jaw, back, epigastrium
• Associated with sweating, nausea, dyspnoea, palpitations
• Pain at rest lasting >20 minutes (STEMI); may be crescendo/at rest (unstable angina/NSTEMI)

Atypical Presentations (Common in Elderly, Women, Diabetics)

• Epigastric pain, isolated dyspnoea, syncope, confusion
• Silent MI - particularly in diabetic neuropathy
• Painless troponin elevation - consider type 2 MI

ECG Classification

• STEMI: ≥2mm ST elevation in V1-V3, or ≥1mm in 2 contiguous limb leads; new LBBB
• NSTEMI: ST depression, T-wave inversion, or normal ECG with positive troponin
• Unstable angina: ECG changes without troponin rise

Red Flags

• ST elevation on ECG - activate primary PCI pathway immediately
• Cardiogenic shock (hypotension, pulmonary oedema, poor perfusion) - highest mortality, may need mechanical support
• Acute mitral regurgitation, VSD, or free wall rupture - mechanical complications requiring emergency surgery
• Ventricular arrhythmias (VT/VF) - immediate defibrillation

Bedside

• 12-lead ECG: Within 10 minutes of presentation - repeat at 15-30 min if initial normal and pain continues
• Observations: BP (both arms), HR, SpO2, RR
• Pain assessment: Onset, character, radiation, severity

Bloods

• High-sensitivity troponin (hs-cTnI or hs-cTnT): At presentation and 3 hours (or 0 and 1 hour with validated rapid rule-out protocol)
• FBC: Anaemia (type 2 MI), baseline
• U&Es: Renal function (pre-PCI, drug dosing)
• Glucose/HbA1c: Diabetes screening
• Lipid profile: Within 24 hours (most accurate before acute phase response)
• Coagulation: Pre-anticoagulation

Imaging

• CXR: Pulmonary oedema, mediastinal widening (dissection)
• Echocardiography: Assess LV function, regional wall motion abnormalities, mechanical complications
• Coronary angiography: Primary PCI for STEMI; within 72 hours for NSTEMI (within 24h if high-risk GRACE >140)

Special Tests

• GRACE score: Risk stratification for NSTEMI/UA - guides timing of angiography and intensity of antithrombotic therapy
• CT coronary angiography: For low-intermediate risk chest pain with indeterminate troponin

Non-pharmacological

• Primary PCI for STEMI: Within 120 minutes of first medical contact - activate catheter lab immediately
• Oxygen: Only if SpO2 <94% (DETO2X-AMI trial - routine O2 not beneficial in normoxic patients)
• Cardiac monitoring: Continuous until diagnosis established

Pharmacological

Immediate (all ACS):

• Aspirin 300mg PO (chewed for rapid absorption)
• GTN: Sublingual 400mcg spray (if SBP >90mmHg; avoid in RV infarction)
• Morphine 2-5mg IV: If ongoing pain (with metoclopramide 10mg IV antiemetic) - use cautiously

STEMI - Primary PCI pathway:

• Aspirin 300mg + ticagrelor 180mg (or prasugrel 60mg if ticagrelor contraindicated)
• Unfractionated heparin during PCI (70-100 units/kg IV)
• GP IIb/IIIa inhibitor (abciximab or eptifibatide) - if needed during PCI
• If PCI not available within 120 min: Thrombolysis (alteplase, tenecteplase, or reteplase)

NSTEMI/UA:

• Aspirin 300mg + ticagrelor 180mg loading then 90mg BD (or clopidogrel 300mg loading then 75mg OD)
• Fondaparinux 2.5mg SC OD (or LMWH if proceeding to PCI within 24h)
• Angiography timing guided by GRACE score: >140 = within 24h; 109-140 = within 72h; <109 = conservative or elective

Secondary prevention (all ACS):

• DAPT for 12 months (aspirin 75mg + ticagrelor 90mg BD)
• Statin: Atorvastatin 80mg OD (start immediately)
• ACEi: Ramipril 1.25-10mg OD (start within 24h if LV impairment)
• Beta-blocker: Bisoprolol 1.25-10mg OD
• Cardiac rehabilitation referral

Surgical/Interventional

• Primary PCI: Drug-eluting stent placement
• Thrombolysis: If PCI not available within 120 min - tenecteplase weight-adjusted IV bolus
• CABG: For left main stem or triple-vessel disease (especially with diabetes)
• Mechanical support: IABP or Impella for cardiogenic shock

Referral Criteria

• STEMI - immediate primary PCI referral (call catheter lab directly)
• NSTEMI with GRACE >140 - urgent angiography within 24h
• Cardiogenic shock - urgent cardiology/cardiac surgery
• Post-MI heart failure - cardiology for optimisation and device assessment

• STEMI primary PCI mortality: ~5-7% at 30 days; significantly better than thrombolysis
• NSTEMI mortality: ~5% at 30 days; ~12% at 1 year
• Door-to-balloon time <90 min: Associated with best outcomes
• Risk factors for poor outcome: Age, diabetes, renal failure, heart failure, anterior STEMI, late presentation
• Long-term: 10-year survival post-MI ~70% with optimal secondary prevention
• Cardiac rehabilitation: Reduces mortality by 20-25%

GRACE Score Risk Stratification

ECG Localisation of STEMI

Key ACS Trials

Key Facts

Stroke thrombolysis has revolutionised the emergency management of ischaemic stroke since the landmark NINDS trial (1995). The addition of mechanical thrombectomy has further improved outcomes for large vessel occlusion. Time remains the most critical factor - 'time is brain'.

Epidemiology

Stroke affects approximately 100,000 people per year in the UK. Ischaemic stroke accounts for 85%, haemorrhagic stroke 15%. Approximately 12% of ischaemic stroke patients in the UK receive thrombolysis (SSNAP data). Stroke is the 4th leading cause of death and the leading cause of adult disability in the UK.

Aetiology

Ischaemic stroke results from:

• Large artery atherosclerosis (carotid, intracranial) - ~25%
• Cardioembolism (AF, valvular disease, LV thrombus) - ~25%
• Small vessel disease (lacunar) - ~25%
• Other/undetermined - ~25%

Pathophysiology

Acute vessel occlusion creates an ischaemic core (irreversibly damaged) surrounded by a penumbra (ischaemic but potentially salvageable tissue). The penumbra relies on collateral blood supply and is the target of reperfusion therapy. Without treatment, the penumbra progressively converts to infarct core - approximately 1.9 million neurones lost per minute of untreated large vessel occlusion.

Stroke Recognition (FAST)

• Face: Facial weakness (drooping)
• Arms: Arm weakness (drift)
• Speech: Slurred or absent speech
• Time: Time to call 999

NIHSS (National Institutes of Health Stroke Scale)

• Quantifies stroke severity (0-42)
• Score >5 - moderate stroke, consider thrombolysis
• Score >10 - moderate-severe, high likelihood of large vessel occlusion
• Score >20 - severe stroke

Large Vessel Occlusion (LVO) Signs

• Dense hemiplegia, hemisensory loss
• Neglect, gaze preference
• Aphasia (dominant hemisphere)
• NIHSS typically ≥6

Red Flags

• Rapidly improving symptoms - may still benefit from thrombolysis (don't assume TIA)
• Seizure at onset - difficult to distinguish from stroke; CT/MRI helps
• Posterior circulation stroke - may present with vertigo, ataxia, visual loss, dysphagia (often missed)
• Young stroke - consider dissection, PFO, thrombophilia, cocaine

Bedside

• CT head (non-contrast): IMMEDIATELY - to exclude haemorrhage (must be done before thrombolysis)
• Blood glucose: Exclude hypoglycaemia (stroke mimic)
• NIHSS score: Quantify severity, track response
• ECG: AF detection
• Observations: BP - must be <185/110 before thrombolysis

Bloods

• FBC, coagulation (INR, APTT): Must check before thrombolysis (but do NOT delay treatment for results unless on anticoagulants)
• U&Es, glucose: Baseline
• Troponin: Concurrent MI in some patients

Imaging

• CT angiography (CTA): Identify large vessel occlusion - essential for thrombectomy decision
• CT perfusion: Identify ischaemic penumbra - guides late thrombectomy (DAWN/DEFUSE-3 criteria)
• MRI (DWI/PWI): Most sensitive for early ischaemia; DWI-FLAIR mismatch can help time unknown-onset strokes

Special Tests

• Carotid USS/CTA: After acute phase - assess for carotid stenosis
• Echocardiography: Cardioembolic source (PFO, thrombus, valve disease)
• 24h/72h Holter or prolonged ECG: Paroxysmal AF detection

Non-pharmacological

• Stroke unit admission: All stroke patients - reduces mortality by 20% (Stroke Unit Trialists' Collaboration)
• Swallow screen: Before any oral intake - NIHSS, water swallow test; SALT assessment if concerns
• Early mobilisation: Within 24-48 hours (AVERT trial - avoid very early aggressive mobilisation)
• Multidisciplinary team: Physiotherapy, occupational therapy, SALT, nursing, psychology

Pharmacological

Thrombolysis (within 4.5 hours):

• Alteplase 0.9mg/kg IV (max 90mg): 10% as IV bolus, remaining 90% over 60 minutes
• BP must be <185/110 before treatment - use labetalol 10-20mg IV or GTN infusion
• Monitor for sICH: neuro obs every 15 min for 2h, every 30 min for 6h, hourly for 24h
• No antiplatelet or anticoagulant for 24 hours post-thrombolysis

If sICH occurs after thrombolysis:

• Stop alteplase infusion
• Urgent CT head
• Tranexamic acid 1g IV, cryoprecipitate 10 units, consider platelet transfusion

Secondary prevention (start at 24h post-thrombolysis or immediately if not thrombolysed):

• Aspirin 300mg OD for 14 days, then clopidogrel 75mg OD long-term
• Statin: Atorvastatin 20-80mg OD
• Anticoagulation for AF: DOAC (apixaban 5mg BD, rivaroxaban 20mg OD) - start at 2-14 days depending on infarct size
• Antihypertensive: Target <130/80 after acute phase

Surgical/Interventional

• Mechanical thrombectomy: For LVO (ICA/M1 MCA) within 6 hours (or up to 24h with favourable perfusion imaging)
• Decompressive craniectomy: For malignant MCA infarction with cerebral oedema (within 48h, age ≤60) - DECIMAL/DESTINY/HAMLET trials
• Carotid endarterectomy/stenting: For symptomatic carotid stenosis >50% (ECST criteria) - within 2 weeks of index event

Referral Criteria

• All suspected stroke - emergency ambulance to nearest HASU (Hyper-Acute Stroke Unit)
• LVO identified - refer to thrombectomy centre (neurosciences centre)
• Carotid stenosis >50% - vascular surgery within 2 weeks

• Thrombolysis at 3 hours: NNT 7 for favourable outcome; absolute benefit ~12%
• Thrombolysis at 4.5 hours: NNT 14; absolute benefit ~7%
• Thrombectomy: NNT 2.6 for reduced disability in LVO (MR CLEAN, ESCAPE, EXTEND-IA trials)
• sICH risk: ~6% with thrombolysis; mortality from sICH ~50%
• Overall stroke 30-day mortality: ~12%; 1-year mortality ~25%
• Stroke unit care: Reduces mortality by 20% and disability by 15% compared with general ward care

Thrombolysis Inclusion/Exclusion Criteria (Summary)

Key Stroke Thrombolysis/Thrombectomy Trials

Key Facts

Acute stroke management requires an integrated system response from emergency services to specialist stroke units. The UK has developed a highly effective hyper-acute stroke pathway that has significantly improved outcomes over the past 15 years.

Epidemiology

Stroke affects approximately 100,000 people per year in the UK. It is the 4th leading cause of death (~34,000 deaths/year) and the leading cause of adult disability. Ischaemic stroke accounts for 85%, intracerebral haemorrhage 10%, and subarachnoid haemorrhage 5%. The UK stroke mortality rate has halved over the past 20 years.

Aetiology

Ischaemic stroke (85%):

• Large artery atherosclerosis (25%)
• Cardioembolism (25%) - AF, valvular disease
• Small vessel disease/lacunar (25%)
• Other/cryptogenic (25%) - dissection, PFO, thrombophilia

Haemorrhagic stroke (15%):

• Intracerebral haemorrhage: Hypertension (most common), amyloid angiopathy, anticoagulation, AVM
• Subarachnoid haemorrhage: Berry aneurysm rupture (85%), AVM, perimesencephalic

Pathophysiology

Ischaemic stroke: Acute vessel occlusion creates an ischaemic core (irreversible) and penumbra (salvageable). Reperfusion therapy targets the penumbra. Without intervention, the penumbra converts to infarct over hours. Cerebral oedema peaks at 3-5 days and may cause herniation in large infarcts.

Haemorrhagic stroke: Vessel rupture causes parenchymal haematoma with mass effect. Haematoma expansion in the first hours worsens outcome. Perihematomal oedema adds to mass effect. Blood products in CSF cause vasospasm (SAH) and hydrocephalus.

Ischaemic Stroke Syndromes

• Anterior circulation (MCA): Contralateral hemiparesis (face + arm > leg), hemisensory loss, homonymous hemianopia, aphasia (dominant) or neglect (non-dominant)
• Anterior circulation (ACA): Contralateral leg weakness > arm, personality change
• Posterior circulation: Vertigo, diplopia, visual field loss, ataxia, dysphagia, dysarthria, crossed signs
• Lacunar syndromes: Pure motor, pure sensory, ataxic hemiparesis, dysarthria-clumsy hand

Haemorrhagic Stroke

• Sudden severe headache (thunderclap in SAH)
• Rapid deterioration, vomiting, reduced consciousness
• Focal neurology depending on location
• SAH: Neck stiffness, photophobia, III/VI nerve palsy

Red Flags

• Thunderclap headache - SAH until proven otherwise (CT + LP if CT negative at <12h)
• Rapid neurological deterioration - haemorrhagic transformation, cerebral oedema, re-occlusion
• GCS deterioration - consider repeat CT, neurosurgical referral
• Posterior circulation stroke signs - frequently missed; requires high clinical suspicion

Bedside

• CT head (non-contrast): Immediately if thrombolysis candidate; within 1 hour for all strokes
• Blood glucose: Exclude hypoglycaemia
• NIHSS: Quantify severity
• ECG: AF detection
• Swallow screen: Before any oral intake

Bloods

• FBC, coagulation, U&Es, glucose, lipids: Baseline
• HbA1c: Diabetes screening
• Troponin: Co-existent MI

Imaging

• CT angiography: Identify LVO for thrombectomy; carotid stenosis assessment
• CT perfusion: Guide late thrombectomy decisions (penumbra assessment)
• MRI (DWI/FLAIR): Most sensitive for acute ischaemia; DWI-FLAIR mismatch for wake-up strokes
• Carotid USS: Non-invasive assessment of carotid stenosis

Special Tests

• Echocardiography (TTE ± TOE): Cardioembolic source - PFO, valve disease, LV thrombus
• Prolonged cardiac monitoring: 24-72h Holter or implantable loop recorder for paroxysmal AF
• Thrombophilia screen: Young stroke (<55) without obvious cause

Non-pharmacological

• Stroke unit care: All patients - reduces mortality and disability (Stroke Unit Trialists' Collaboration)
• Swallowing assessment: Within 4 hours of admission; SALT if concerns
• DVT prophylaxis: IPC/TEDS (NOT anticoagulants in first 14 days for large ischaemic or haemorrhagic stroke)
• Positioning: Avoid flat positioning in first 24h if aspiration risk
• Early rehabilitation: Within 24-48h - PT, OT, SALT, psychology
• Nutrition: Enteral feeding (NG tube) if unsafe swallow persists >24-48h

Pharmacological

Ischaemic stroke:

• Aspirin 300mg within 24 hours (after CT excludes haemorrhage); continue for 14 days then clopidogrel 75mg OD
• Thrombolysis: Alteplase 0.9mg/kg IV if within 4.5 hours
• Secondary prevention: Statin (atorvastatin 20-80mg), antihypertensive (target <130/80 after acute phase), anticoagulation for AF (DOAC)

Haemorrhagic stroke:

• BP control: SBP <140 mmHg within 1 hour (IV labetalol or GTN infusion) - INTERACT2 trial
• Reverse anticoagulation: Warfarin - IV vitamin K 10mg + prothrombin complex concentrate (Beriplex); DOAC - idarucizumab for dabigatran, andexanet alfa for factor Xa inhibitors
• Tranexamic acid 1g IV: Consider within 3 hours (TICH-2 trial - modest benefit)
• Avoid antiplatelet/anticoagulant for 1-2 weeks minimum

Surgical/Interventional

• Thrombectomy: LVO within 6h (or 24h with perfusion imaging)
• Decompressive craniectomy: Malignant MCA infarction (age ≤60, within 48h)
• Neurosurgical evacuation: Cerebellar haemorrhage >3cm or with hydrocephalus/deterioration
• EVD: For acute hydrocephalus (SAH, IVH)
• Carotid endarterectomy: Symptomatic stenosis >50% within 2 weeks

Referral Criteria

• All suspected strokes - emergency ambulance to HASU
• LVO - thrombectomy centre
• Cerebellar/large haemorrhage - neurosurgery
• Symptomatic carotid stenosis - vascular surgery within 2 weeks

• 30-day mortality: Ischaemic ~12%, ICH ~30-40%, SAH ~30-50%
• 1-year mortality: ~25% overall for all stroke types
• Stroke unit care: Reduces death AND disability - NNT 20 for one additional patient alive and independent
• Post-stroke disability: ~50% of survivors have some residual disability; 30% require help with ADLs
• Stroke recurrence: ~10% in first year without secondary prevention; anticoagulation for AF reduces stroke by ~65%
• Thrombectomy: NNT 2.6 for reduced disability in LVO

NIHSS Score Components

SSNAP Key Performance Indicators

Key Stroke Trials

Key Facts

Sepsis is a medical emergency requiring the same urgency of response as cardiac arrest or major trauma. The UK Sepsis Trust estimates that early recognition and treatment could save 14,000 lives per year in the UK. Structured assessment tools and protocolised care pathways have significantly improved outcomes.

Epidemiology

Sepsis affects approximately 48,000 people per year in England, with approximately 26,000 deaths attributed to sepsis. It accounts for approximately 2% of all hospital admissions. Global sepsis incidence is approximately 49 million cases per year with 11 million deaths (Lancet 2020). Sepsis mortality has improved from ~50% to ~25-30% over the past 20 years.

Aetiology

Common sources of infection:

• Respiratory (pneumonia) - most common (~40%)
• Urinary tract (~20%)
• Abdominal (peritonitis, cholangitis, diverticulitis) (~15%)
• Skin/soft tissue (cellulitis, necrotising fasciitis) (~10%)
• Line-related/healthcare-associated (~10%)
• Unknown source (~5%)

Common organisms: Gram-negative (E. coli, Klebsiella, Pseudomonas), Gram-positive (S. aureus, S. pneumoniae, Streptococcus spp.); polymicrobial in abdominal sepsis

Pathophysiology

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection (Sepsis-3 definition). The pathophysiology involves:

• Immune dysregulation: Pro-inflammatory (TNF-α, IL-1, IL-6) and anti-inflammatory mediators causing tissue damage AND immunosuppression simultaneously
• Endothelial dysfunction: Increased vascular permeability, microvascular thrombosis, vasodilation
• Organ dysfunction: Occurs through microcirculatory failure, mitochondrial dysfunction, and cellular injury
• Septic shock: Sepsis with persistent hypotension requiring vasopressors AND lactate >2 mmol/L despite adequate fluid resuscitation

Sepsis Screening (Red Flag Criteria - NICE NG51)

High risk (any one of - amber/red flag):

• Systolic BP ≤90 mmHg or drop >40 from baseline
• Heart rate >130/min
• Respiratory rate ≥25/min
• Temperature <36°C
• New confusion or altered mental state
• Lactate >2 mmol/L
• Non-blanching rash (meningococcal/purpura fulminans)
• Urine output <0.5 mL/kg/hr

Septic Shock

• Persistent hypotension despite adequate fluid resuscitation (≥30 mL/kg crystalloid)
• Requiring vasopressors to maintain MAP ≥65 mmHg
• Lactate >2 mmol/L despite resuscitation
• Warm peripheries (early/hyperdynamic) → cool, mottled (late/hypodynamic)

Red Flags

• NEWS2 ≥7 or single parameter 3 - trigger urgent review
• Lactate >4 mmol/L - high mortality, ICU referral
• Purpuric/non-blanching rash - consider meningococcal sepsis
• Neutropenic sepsis (WCC <0.5 × 10⁹/L) - immediate IV antibiotics per local protocol
• Immunosuppressed patients - low threshold for sepsis screening

Bedside

• NEWS2 score: Trigger for sepsis screening
• Lactate (VBG/ABG): Immediate - guide severity and resuscitation response
• Blood glucose: Hypoglycaemia or hyperglycaemia
• Urine output: Catheterise - target >0.5 mL/kg/hr
• Point-of-care USS: Assess fluid status, cardiac function, source (e.g., hydronephrosis, ascites)

Bloods

• Blood cultures (×2 sets): Before antibiotics - aerobic and anaerobic bottles from separate sites
• FBC: WCC (leucocytosis or leucopenia), platelets (DIC)
• U&Es: AKI (rising creatinine)
• LFTs, bilirubin: Hepatic dysfunction
• Coagulation + fibrinogen: DIC screening
• CRP: Inflammatory marker (non-specific)
• Procalcitonin: More specific for bacterial infection; guides antibiotic duration

Imaging

• CXR: Pneumonia source
• CT abdomen: Intra-abdominal source (perforation, abscess, cholangitis)
• Renal USS: Obstructed infected system (pyonephrosis)

Special Tests

• Urine MC&S: UTI source
• Wound swab/tissue culture: Soft tissue source
• Lumbar puncture: If meningitis suspected (after CT if raised ICP concerns)
• SOFA score: Quantifies organ dysfunction (≥2 increase defines sepsis)

Non-pharmacological

• Sepsis 6 within 1 hour: Give O2, Give IV fluids, Give IV antibiotics, Take blood cultures, Measure lactate, Measure urine output
• Source control: Essential - drain abscess, remove infected device, debride wound, relieve obstruction

Pharmacological

Fluid resuscitation:

• IV crystalloid 500mL bolus (20mL/kg in children); assess response; repeat up to 30mL/kg in first 3 hours
• Reassess after each bolus - avoid fluid overload

Antibiotics (within 1 hour):

• Empiric broad-spectrum: Per local trust guidelines (e.g., piperacillin-tazobactam 4.5g IV TDS or meropenem 1g IV TDS for severe/source unknown)
• Community-acquired pneumonia: Co-amoxiclav 1.2g IV + clarithromycin 500mg IV
• UTI: Co-amoxiclav 1.2g IV or gentamicin per local protocol
• Neutropenic sepsis: Piperacillin-tazobactam 4.5g IV TDS (per NICE NG151)
• Narrow spectrum based on culture results; review at 48-72h

Vasopressors (if fluid-resistant hypotension):

• Noradrenaline: First-line - 0.05-1 mcg/kg/min (via central line) to target MAP ≥65 mmHg
• Vasopressin 0.03 units/min: Adjunct if noradrenaline alone insufficient
• Hydrocortisone 200mg/day: If vasopressor-dependent despite adequate fluids (ADRENAL trial - no mortality benefit but faster shock resolution)

Surgical/Interventional

• Source control: Priority - interventional radiology drainage, laparotomy, nephrostomy, debridement
• Renal replacement therapy: For AKI with refractory hyperkalaemia, acidosis, or fluid overload

Referral Criteria

• NEWS2 ≥7 or lactate >4 - ICU referral
• Vasopressor-dependent hypotension - ICU admission
• Neutropenic sepsis - haematology and infectious diseases
• Failure to respond to initial resuscitation - senior review and ICU

• Sepsis mortality: ~25-30% overall; septic shock ~30-40%
• Each hour delay in antibiotics increases mortality by ~7.6%
• Sepsis 6 compliance: Reduces mortality by approximately 20%
• Lactate clearance >10% at 6 hours: Associated with improved survival
• Post-sepsis syndrome: ~40% of survivors have physical/psychological sequelae at 1 year
• 30-day readmission: ~20% - often due to recurrent infection or deconditioning

Sepsis Six Bundle

SOFA Score (Sequential Organ Failure Assessment)

Increase ≥2 from baseline = sepsis (Sepsis-3 definition).

Key Sepsis Trials

Key Facts

Major trauma is a time-critical condition requiring a systematic team approach. The UK Major Trauma Network, established in 2012, has significantly improved outcomes through regionalised care with dedicated major trauma centres.

Epidemiology

Major trauma affects approximately 20,000 people per year in England. It is the leading cause of death in those aged 1-40 years and a leading cause of disability. Road traffic collisions account for approximately 40%, falls 40%, and violence/other 20%. The establishment of the UK Trauma Network has reduced preventable death rates from approximately 30% to <5%.

Aetiology

Mechanism of injury:

• Blunt trauma (90% in UK): RTC, falls, assaults, sports
• Penetrating trauma (10%): Stab wounds, gunshot wounds
• Blast injuries: Explosive devices - primary (blast wave), secondary (fragments), tertiary (displacement), quaternary (burns, crush)

Pathophysiology

Trauma causes tissue injury, haemorrhage, and a systemic inflammatory response. The lethal triad of hypothermia, acidosis, and coagulopathy is the primary driver of mortality in bleeding trauma patients. Damage control resuscitation aims to prevent and treat this triad. Traumatic brain injury is the leading cause of death in polytrauma.

Primary Survey (ABCDE)

• A (Airway with C-spine protection): Assess patency, clear debris, jaw thrust, consider intubation. Assume C-spine injury until cleared.
• B (Breathing): Inspect, palpate, percuss, auscultate. Treat tension pneumothorax, open pneumothorax, massive haemothorax, flail chest immediately.
• C (Circulation with haemorrhage control): Direct pressure on external bleeding. Assess for shock (tachycardia, hypotension, cold peripheries). Two large-bore IV cannulae. Start fluid/blood resuscitation.
• D (Disability): GCS, pupil assessment, blood glucose, lateralising signs
• E (Exposure and Environment): Fully expose, log-roll, maintain temperature (warm blankets, warm fluids, warm environment)

Life-Threatening Injuries (Primary Survey)

• Airway obstruction, tension pneumothorax, open pneumothorax
• Massive haemothorax, flail chest with pulmonary contusion
• Cardiac tamponade
• Massive haemorrhage (external or internal)

Red Flags

• GCS drop of ≥2 points - repeat CT head, consider neurosurgical emergency
• Haemodynamic instability not responding to initial resuscitation - consider ongoing haemorrhage, activate massive transfusion
• Mechanism involving high energy transfer - maintain high suspicion for occult injuries
• Abdominal distension with shock - intra-abdominal haemorrhage, consider emergency laparotomy

Bedside

• Primary survey: Clinical assessment is the first 'investigation'
• FAST (Focused Assessment with Sonography for Trauma): Free fluid in abdomen, pericardium; haemothorax
• GCS: Serial assessment
• Blood glucose: Capillary

Bloods

• FBC, U&Es, coagulation, fibrinogen: Baseline
• Group and crossmatch: At least 4 units; activate MHP if needed
• Lactate: Tissue perfusion marker
• ABG/VBG: pH, base deficit, Hb, K⁺
• Point-of-care coagulation (TEG/ROTEM): Guide transfusion in massive haemorrhage

Imaging

• CXR: Pneumothorax, haemothorax, mediastinal widening, rib fractures
• AP pelvis X-ray: Pelvic fracture assessment
• CT trauma series: CT head, C-spine, chest, abdomen, pelvis - after primary survey stabilisation
• CT angiography: If vascular injury suspected

Special Tests

• Diagnostic peritoneal lavage (DPL): Rarely used now (replaced by FAST and CT)
• Focused neurovascular exam: Before and after any fracture manipulation

Non-pharmacological

• ATLS primary survey and resuscitation: Simultaneous assessment and treatment
• C-spine immobilisation: Until cleared clinically or by imaging
• Haemorrhage control: Direct pressure, tourniquets (extremity), pelvic binder, splints
• Temperature management: Warm fluids, blankets, warm theatre - prevent hypothermia
• Log-roll: Assess posterior injuries (C-spine, thoracolumbar spine, perineum)

Pharmacological

• Tranexamic acid 1g IV within 3 hours of injury (CRASH-2 trial) - reduces bleeding death by ~30%
• Massive transfusion protocol (1:1:1): pRBC:FFP:Platelets; target fibrinogen >1.5g/L (cryoprecipitate)
• Permissive hypotension: Target SBP 80-90 mmHg until surgical haemorrhage control (avoid in TBI - target SBP >110 in head injury)
• Antibiotics: For open fractures (co-amoxiclav 1.2g IV ± gentamicin for grade III), penetrating abdominal injuries
• Tetanus prophylaxis: For open wounds - check immunisation status
• VTE prophylaxis: LMWH when safe (balance against bleeding risk)

Surgical/Interventional

• Emergency thoracotomy: Penetrating chest trauma with cardiac arrest or imminent arrest
• Emergency laparotomy: Haemodynamically unstable abdominal trauma
• Interventional radiology: Embolisation for pelvic, hepatic, splenic haemorrhage
• External fixation: Pelvic fracture stabilisation
• Chest drain: Haemothorax, pneumothorax

Referral Criteria

• Major trauma (ISS ≥16) - major trauma centre
• Head injury with GCS ≤8 or deterioration - neurosurgery
• Spinal cord injury - spinal injuries centre
• Vascular injury - vascular surgery
• Burns >10% TBSA - burns centre

• Major trauma centre care: 20-25% mortality reduction compared with non-MTC care (TARN data)
• Preventable deaths: <5% in mature trauma systems (UK improved from ~30% to <5% since 2012)
• TBI: Leading cause of trauma death and disability; GCS ≤8 carries ~30% mortality
• Damage control resuscitation: Has significantly improved survival in haemorrhagic shock
• Rehabilitation: Early, structured rehabilitation improves functional outcomes; many trauma survivors require long-term support

ATLS Classification of Haemorrhagic Shock

Damage Control Resuscitation Principles

Key Facts

Major haemorrhage is one of the most time-critical emergencies in medicine. A structured approach with early activation of the massive transfusion protocol, damage control resuscitation, and rapid source control saves lives.

Epidemiology

Major haemorrhage occurs in trauma, obstetrics (postpartum haemorrhage), gastrointestinal bleeding, surgical complications, and ruptured aortic aneurysms. Haemorrhage is the leading cause of preventable death in trauma. In the UK, massive transfusion protocols are activated thousands of times annually.

Aetiology

• Trauma: Solid organ injury (liver, spleen), vascular injury, pelvic fracture, long bone fractures
• Obstetric: Postpartum haemorrhage (uterine atony, placenta praevia, abruption, uterine rupture)
• GI: Variceal bleeding, peptic ulcer, aorto-enteric fistula
• Surgical: Post-operative bleeding, vascular surgery complications
• Vascular: Ruptured AAA, aortic dissection
• Coagulopathy: Anticoagulant-related, DIC, haemophilia

Pathophysiology

Massive blood loss leads to the lethal triad: hypothermia (from exposure and cold fluids), acidosis (from tissue hypoperfusion and anaerobic metabolism), and coagulopathy (from dilution, consumption, and hypothermia). This creates a vicious cycle where coagulopathy worsens bleeding, which worsens acidosis and hypothermia. Damage control resuscitation aims to break this cycle.

Clinical Features of Major Haemorrhage

• Tachycardia (earliest sign), hypotension, tachypnoea
• Cold, pale, clammy peripheries; prolonged capillary refill
• Altered mental status (confusion → unconsciousness)
• Oliguria/anuria
• Visible external bleeding or signs of internal bleeding (abdominal distension, chest drain output, PV bleeding)

Shock Index

• Shock index = HR/SBP: Normal <0.7; >1.0 indicates significant haemorrhage

Red Flags

• Patient not responding to initial resuscitation - ongoing uncontrolled haemorrhage
• Coagulopathic bleeding (oozing from multiple sites, surgical wounds, IV sites) - DIC or consumptive coagulopathy
• Chest drain output >1500mL initially or >200mL/hr for 2-4h - thoracotomy indication
• Massive PPH (>1000mL) - activate obstetric haemorrhage protocol

Bedside

• ABCDE assessment: Simultaneous assessment and resuscitation
• FAST USS: Free fluid in abdomen/pelvis, haemothorax
• ABG/VBG: Hb, pH, base deficit, lactate, Ca²⁺, K⁺
• Point-of-care coagulation (TEG/ROTEM): Guide blood product therapy in real-time

Bloods

• Group and crossmatch: Urgent - 6 units minimum; O-neg until available
• FBC: Hb (may be normal initially in acute haemorrhage), platelets
• Coagulation: PT, APTT, fibrinogen (target >1.5g/L)
• U&Es, LFTs: Organ function
• Lactate: Tissue perfusion (serial monitoring)
• Calcium: Ionised Ca²⁺ - citrate in blood products causes hypocalcaemia

Imaging

• CXR: Haemothorax, mediastinal widening
• CT (with contrast): Identify bleeding source - CT angiography for active extravasation
• CT angiography: Vascular injury, aortic pathology

Special Tests

• Interventional angiography: Diagnostic and therapeutic embolisation
• OGD: Upper GI bleeding source identification and treatment

Non-pharmacological

• Activate massive transfusion protocol (MTP): Single phone call activates blood bank to release packs
• Haemorrhage control: Direct pressure, tourniquet (extremity), pelvic binder, splints
• Warm patient: Warm fluids (Level 1 rapid infuser), blankets, warm theatre (>24°C)
• Two large-bore IV cannulae or central access: Rapid infusion capability

Pharmacological

• Tranexamic acid 1g IV over 10 min (then 1g over 8h in trauma; or additional 1g in PPH) - within 3 hours
• Blood products (1:1:1 ratio):
  • pRBC: Restore oxygen-carrying capacity
  • FFP: Replace clotting factors (target PT/APTT <1.5× normal)
  • Platelets: Target >75 × 10⁹/L (>100 if head injury)
  • Cryoprecipitate: Target fibrinogen >1.5g/L (give 2 pools = 10 units)
• Calcium chloride 10mL 10% IV: Give per 4 units blood (prevent citrate-induced hypocalcaemia)
• Permissive hypotension: Limit crystalloid to 1-2L initially; target SBP 80-90 (NOT in TBI)
• Reversal agents (anticoagulant-related bleeding):
  • Warfarin: Vitamin K 5-10mg IV + PCC (Beriplex 25-50 IU/kg)
  • Dabigatran: Idarucizumab 5g IV
  • Factor Xa inhibitors: Andexanet alfa (if available) or PCC

Surgical/Interventional

• Damage control surgery: Control haemorrhage and contamination; temporary closure
• Interventional radiology: Embolisation (pelvic, hepatic, splenic bleeding)
• Emergency thoracotomy: Penetrating chest trauma with cardiac arrest
• Emergency laparotomy: Abdominal haemorrhage in unstable patient
• Endoscopy: GI bleeding - clip, injection, banding

Referral Criteria

• Activate MTP - call blood bank (usually single-number activation)
• Surgical source not controlled - urgent surgical team
• Interventional radiology - if available, for angiographic embolisation
• Massive PPH - obstetric team, anaesthetist, consider cell salvage

• Mortality from major haemorrhage: Varies widely by cause - trauma ~40% for class IV shock, PPH ~1%
• 1:1:1 transfusion ratio: PROPPR trial showed improved haemostasis; trend towards reduced mortality
• Tranexamic acid within 1 hour: Reduces bleeding death by ~30% (CRASH-2)
• Damage control resuscitation: Has transformed survival from haemorrhagic shock
• Complications of massive transfusion: Hypocalcaemia, hyperkalaemia, hypothermia, TRALI, TACO, transfusion reactions

Massive Transfusion Protocol - Typical Pack

Targets During Major Haemorrhage

Key Haemorrhage Trials

Key Facts

Head injury is one of the most common reasons for emergency department attendance. The vast majority are mild, but identifying patients at risk of significant intracranial pathology is critical. Traumatic brain injury (TBI) is the leading cause of death and disability in adults under 40.

Epidemiology

Approximately 1.4 million head injury attendances per year in England and Wales. ~200,000 require admission. ~5,000 deaths per year from TBI. Falls are the most common mechanism in all ages; RTCs are the most common mechanism in young adults. Male:female ratio is 2:1.

Aetiology

• Falls: Most common overall (especially elderly)
• Road traffic collisions: Most common in 15-30 age group
• Assaults: Common in young men
• Sports: Rugby, horse-riding, cycling
• Non-accidental injury: Consider in children with unexplained or inconsistent injuries

Pathophysiology

Primary brain injury: Occurs at the time of impact - contusion, diffuse axonal injury (DAI), intracranial haemorrhage. Largely irreversible.

Secondary brain injury: Develops hours to days after - caused by hypoxia, hypotension, raised ICP, cerebral oedema, seizures, infection. The focus of management is to PREVENT secondary injury.

Raised ICP: Monro-Kellie doctrine - fixed cranial volume means any increase in one compartment (blood, brain, CSF) must be compensated or ICP rises. Normal ICP 5-15 mmHg. CPP = MAP − ICP; target CPP >60 mmHg.

GCS Assessment

Severity Classification

• Mild: GCS 13-15
• Moderate: GCS 9-12
• Severe: GCS 3-8 (requires intubation and ventilation)

Intracranial Haemorrhage Types

• Extradural: Lucid interval, middle meningeal artery, biconvex on CT, rapid deterioration
• Acute subdural: Crescent-shaped, bridging veins, associated brain injury, high mortality
• Subarachnoid: Traumatic or spontaneous, blood in sulci/cisterns
• Intracerebral contusion/haemorrhage: Coup and contrecoup injuries

Red Flags (NICE CG176 - Immediate CT)

• GCS <13 at any point since injury
• GCS <15 at 2 hours after injury
• Suspected skull fracture (open, depressed, base of skull)
• Post-traumatic seizure
• Focal neurological deficit
• ≥2 episodes of vomiting
• On anticoagulants/bleeding disorder

Bedside

• GCS: Serial assessment (every 30 min initially, increase frequency if deteriorating)
• Pupil assessment: Size, reactivity, asymmetry - unilateral fixed dilated pupil = uncal herniation
• Blood glucose: Exclude hypoglycaemia
• C-spine assessment: Assume injury until cleared

Bloods

• FBC, U&Es, coagulation (INR): Baseline and guide anticoagulant reversal
• Group and save: If surgical intervention anticipated
• Blood alcohol/toxicology: If intoxication suspected (may confound GCS)

Imaging

• CT head (non-contrast): Gold standard - as per NICE CG176 criteria
• CT C-spine: For all patients with GCS <13, intubated, or with risk factors per NICE
• CT angiography: If vascular injury suspected (e.g., skull base fracture near carotid canal)
• MRI brain: For diffuse axonal injury (more sensitive than CT), posterior fossa lesions, and prognostication

Special Tests

• ICP monitoring: Intraparenchymal bolt or EVD - for severe TBI (GCS ≤8 with abnormal CT)
• EEG: If seizures suspected
• CT perfusion/Xenon CT: Research/specialist use for cerebral blood flow assessment

Non-pharmacological

• ABCDE assessment: As per ATLS primary survey
• C-spine immobilisation: Until cleared
• Head-up positioning: 30° to aid venous drainage and reduce ICP
• Avoid secondary insults: Maintain normoxia (PaO2 >13 kPa), normocapnia (PaCO2 4.5-5.0 kPa), normothermia, normoglycaemia
• Target SBP >110 mmHg: Hypotension is devastating in TBI

Pharmacological

• Anticoagulant reversal: Warfarin - vitamin K 5-10mg IV + PCC (Beriplex); DOAC - idarucizumab (dabigatran) or andexanet alfa (factor Xa inhibitors)
• Mannitol 20% (0.25-1g/kg IV) or hypertonic saline 3-5% (2-5mL/kg): For acute raised ICP/herniation - temporising measure
• Anti-epileptics: Levetiracetam 500mg-1g IV or phenytoin 15-18mg/kg IV - for post-traumatic seizures (not routine prophylaxis beyond 7 days)
• Analgesia: Paracetamol 1g QDS; avoid NSAIDs (bleeding risk); codeine for moderate pain
• VTE prophylaxis: Balance bleeding risk - LMWH typically started after 24-48h if stable on repeat imaging

Surgical/Interventional

• Emergency craniotomy: Extradural haematoma (>30mL or midline shift >5mm), acute SDH with midline shift
• Decompressive craniectomy: Refractory raised ICP (RESCUEicp trial - improves survival but increases severe disability)
• EVD (External Ventricular Drain): For acute hydrocephalus
• ICP monitoring: For GCS ≤8 with abnormal CT - target ICP <22 mmHg

Referral Criteria

• GCS ≤8 - neurosurgical referral and ICU
• Intracranial haemorrhage requiring surgery - neurosurgery
• Skull fracture (depressed, base of skull) - neurosurgical assessment
• Deteriorating GCS - urgent repeat CT and neurosurgical consultation
• All children with non-accidental injury concerns - safeguarding referral

• Mild TBI (GCS 13-15): >95% make good recovery; ~15% have persistent post-concussion symptoms at 3 months
• Moderate TBI (GCS 9-12): ~80% survive; many have significant disability
• Severe TBI (GCS 3-8): Mortality ~30-40%; ~50% of survivors have moderate-severe disability
• Extradural haematoma: Excellent prognosis if operated early (mortality <5%); poor if late (herniation)
• Acute subdural: Mortality ~50-60%; depends on degree of underlying brain injury
• Diffuse axonal injury: Leading cause of persistent vegetative state post-TBI

NICE CG176 CT Head Criteria

GCS and TBI Severity

Base of Skull Fracture Signs

Key Facts

Cervical spine injury is a potentially devastating consequence of trauma. The goal of assessment is to rapidly identify patients who need imaging while safely clearing the C-spine in low-risk patients. Prevention of secondary cord injury through appropriate immobilisation and management is paramount.

Epidemiology

Cervical spine fractures occur in approximately 2-3% of blunt trauma patients. Cervical cord injury occurs in approximately 0.5%. Falls are the most common mechanism in the elderly; RTCs in young adults. C2 is the most commonly fractured vertebra overall. The subaxial C-spine (C5-C7) is the most common level of cord injury.

Aetiology

High-risk mechanisms:

• Road traffic collision >60mph, ejection from vehicle
• Fall from >1 metre or 5 stairs
• Axial loading (diving, rugby)
• Bicycle collision
• Elderly with minor fall (osteoporotic spine)

Specific fracture types:

• C1 (Jefferson fracture): Burst fracture - axial loading
• C2 (Odontoid/dens fracture): Most common C2 fracture; classified by Anderson and D'Alonzo (Type I-III)
• C2 (Hangman's fracture): Bilateral pars interarticularis fracture - hyperextension
• Subaxial fractures: Flexion-distraction, burst, facet dislocations

Pathophysiology

The cervical spine provides structural support and protects the spinal cord. Injury mechanisms include flexion, extension, rotation, compression, and distraction - often combined. Cord injury results from primary mechanical disruption and secondary injury from oedema, ischaemia, and inflammation. The cervical spinal canal is narrowest at C3-C7, making this region vulnerable to cord compression.

Assessment Approach

• Primary survey (ATLS): C-spine immobilisation during airway management

• Canadian C-spine Rules (CCR):

  1. Any high-risk factor? (Age ≥65, dangerous mechanism, paraesthesia in extremities) → CT
  2. Any low-risk factor allowing safe active ROM? (Simple rear-end RTC, sitting in ED, ambulatory, delayed pain onset, no midline tenderness) → assess ROM
  3. Can actively rotate neck 45° left and right? → No imaging needed

• NEXUS Criteria: C-spine can be cleared if ALL 5 criteria met: No midline tenderness, no focal neurological deficit, normal alertness, no intoxication, no painful distracting injury

Neurological Assessment

• Motor and sensory examination of all four limbs
• Anal tone and perianal sensation (sacral sparing)
• Reflexes including bulbocavernosus reflex
• ASIA classification (A-E)

Red Flags

• Midline cervical tenderness with neurological deficit - high suspicion of unstable injury
• Bilateral upper limb weakness > lower limb - central cord syndrome
• Diaphragmatic breathing (paradoxical) - suggests high cervical cord injury (C3-C5 phrenic nerve)
• Priapism - sign of cord injury
• Neurogenic shock (bradycardia + hypotension) - cord injury above T6

Bedside

• Primary survey: ATLS - maintain immobilisation
• Clinical assessment: CCR or NEXUS to determine imaging need
• Neurological examination: Detailed motor, sensory, reflex, anal tone
• ASIA assessment: If neurological deficit present

Bloods

• Standard trauma bloods: FBC, U&Es, coagulation, group and save
• ABG: If respiratory compromise (high cervical injury)

Imaging

• CT C-spine: First-line in trauma - sensitivity >99% for fracture; requested per clinical decision rules
• CT angiography of neck: If fracture involves foramen transversarium (risk of vertebral artery injury)
• MRI C-spine: Indicated for neurological deficit with normal CT, suspected ligamentous injury, or cord compression
• Flexion-extension views: Historical - rarely used acutely now (MRI preferred)

Special Tests

• CT with 3D reconstruction: For complex fractures - surgical planning
• MRI within 24-72 hours: For all patients with neurological deficit
• Formal clearance protocol: For obtunded patients - serial clinical examination ± MRI at 72 hours

Non-pharmacological

• Immobilisation: Scoop stretcher, head blocks with tape/straps; minimise time in rigid collar (pressure sore risk)
• Manual in-line stabilisation (MILS): During airway management - do NOT apply traction
• Log-roll: For examination and repositioning
• Early specialist referral: To spinal surgery for all cervical fractures

Pharmacological

• Analgesia: Paracetamol 1g QDS; opioids cautiously (respiratory depression risk in cord injury)
• Methylprednisolone: NOT routinely recommended (NASCIS trials methodologically flawed; risks outweigh benefits)
• VTE prophylaxis: LMWH once surgical stability confirmed; mechanical prophylaxis from admission
• Vasopressors: Noradrenaline for neurogenic shock (target MAP ≥85 mmHg for 5-7 days)
• Bowel and bladder management: Catheter, laxatives from day 1

Surgical/Interventional

• Surgical fixation: Unstable fractures - anterior or posterior approach depending on injury pattern
• Emergency decompression: For progressive neurological deficit or cord compression on MRI
• Halo vest: External fixation for upper cervical fractures where surgery is not indicated
• Philadelphia collar: Stable fractures during conservative management
• Timing: Early surgery (<24h) increasingly supported for incomplete cord injuries (STASCIS trial)

Referral Criteria

• All cervical fractures - spinal surgery consultation
• Neurological deficit - emergency MRI and spinal surgery
• Unstable fractures - surgical fixation
• Cord injury - specialist spinal cord injury centre transfer when stable
• Obtunded patient with unclear C-spine - protocolised clearance

• Complete cord injury (ASIA A): <5% neurological recovery if still ASIA A at 72h
• Incomplete cord injury: Significant recovery potential - Brown-Séquard best (~90% ambulate), central cord variable
• Odontoid type II fracture: Non-union rate ~40% with collar alone in elderly → surgery often needed
• Jefferson fracture: Generally good prognosis, most treated conservatively
• Bilateral facet dislocation: High rate of complete cord injury (~75%)
• C-spine clearance in alert trauma patient: If CCR negative and full ROM, <0.1% chance of significant injury

Canadian C-Spine Rules Algorithm

Anderson and D'Alonzo Odontoid Fracture Classification

NEXUS Low-Risk Criteria (All 5 Must Be Met to Clear)

Key Facts

Burns are a common emergency presentation requiring rapid assessment of airway safety, burn depth and area, fluid resuscitation, and pain management. UK burns services are regionalised with specialist burns centres for complex injuries.

Epidemiology

Approximately 175,000 people attend UK EDs with burns annually. ~13,000 require hospital admission. ~300 deaths/year from burns and fires. Scalds are the most common mechanism in children; flame burns in adults. House fires account for the majority of deaths.

Aetiology

• Thermal: Scalds (hot liquid/steam), flame, contact (radiator, iron)
• Chemical: Acids, alkalis (alkali burns penetrate deeper)
• Electrical: Low voltage (<1000V) and high voltage (>1000V) - cardiac arrest risk
• Radiation: Sunburn, radiotherapy
• Inhalational: Thermal injury to upper airway, chemical injury to lower airway (CO, cyanide)

Pathophysiology

Burns cause tissue destruction through protein denaturation. Jackson's burn wound model describes three zones: zone of coagulation (irreversible necrosis at centre), zone of stasis (potentially salvageable - goal of resuscitation), and zone of hyperaemia (will recover). Systemic inflammatory response occurs with burns >20% TBSA causing capillary leak, hypovolaemia, and distributive shock.

Burn Depth Assessment

• Superficial (epidermal): Red, painful, no blisters, blanches - heals in 7 days without scarring
• Superficial partial thickness: Blistering, moist, painful, blanches - heals in 14-21 days with minimal scarring
• Deep partial thickness: Mottled pink/white, reduced sensation, sluggish blanching - requires surgery, >3 weeks
• Full thickness: White/waxy/leathery, painless, no blanching, no capillary refill - requires surgery/grafting

TBSA Assessment

• Wallace Rule of Nines (adults)
• Lund and Browder chart (most accurate, especially children)
• Palm method: Patient's palm (including fingers) = ~1% TBSA

Red Flags

• Stridor, hoarseness, soot in sputum - inhalational injury, may need immediate intubation
• Circumferential burns - risk of compartment syndrome (limb), respiratory compromise (chest/abdomen)
• Burns >20% TBSA - systemic response, need aggressive fluid resuscitation
• Electrical burns - cardiac arrhythmias; visible burn may underestimate deep tissue injury
• Non-accidental injury (especially children) - glove/stocking pattern, clear tide marks, delay in presentation

Bedside

• Primary survey (ABCDE): Airway is priority - assess for inhalation injury
• TBSA estimation: Wallace Rule of Nines or Lund and Browder chart
• Depth assessment: Clinical - erythema, blistering, capillary refill, sensation
• Weight: Essential for Parkland formula calculation
• SpO2 and CO-oximetry: Standard pulse oximetry may be falsely normal in CO poisoning

Bloods

• FBC, U&Es: Baseline; haemoconcentration from fluid shifts
• ABG with carboxyhaemoglobin (COHb): If inhalational injury - COHb >10% significant, >25% severe
• Lactate/cyanide level: If smoke inhalation
• CK: Electrical burns - rhabdomyolysis risk
• Group and save: If burns requiring surgery
• Coagulation: DIC risk in extensive burns

Imaging

• CXR: Baseline and for inhalational injury
• ECG: Electrical burns - arrhythmia monitoring for 24h

Special Tests

• Bronchoscopy: Confirm inhalational injury - mucosal oedema, soot, erythema
• Laser Doppler imaging: Objective burn depth assessment (used in burns centres)

Non-pharmacological

• Cooling: Cool running water 20 min within 3h; remove clothing/jewellery; cover with cling film (loosely)
• Airway: Early intubation if suspected inhalational injury - airway oedema can progress rapidly
• Fluid resuscitation (Parkland formula): 4mL × %TBSA × weight (kg) in first 24h; half in first 8h from time of burn, half in next 16h; use Hartmann's solution
• Wound care: Clean, debride loose tissue, apply antimicrobial dressings (e.g., Jelonet, Mepitel, silver-based dressings)
• Temperature: Keep warm - major burns patients lose heat rapidly

Pharmacological

• Analgesia: Paracetamol 1g QDS + opioid (morphine 0.1-0.2mg/kg IV titrated); intranasal diamorphine in children
• Tetanus prophylaxis: Update if required
• Antibiotics: NOT routine prophylaxis - only for confirmed infection
• CO poisoning: High-flow O2 100% via non-rebreather (half-life of COHb drops from 4-6h to 60-90 min)
• Cyanide poisoning: Hydroxocobalamin 5g IV (Cyanokit) if suspected
• VTE prophylaxis: LMWH for immobilised patients with significant burns

Surgical/Interventional

• Escharotomy: For circumferential full-thickness burns - decompress limb or chest
• Fasciotomy: For compartment syndrome (especially electrical burns)
• Surgical debridement and skin grafting: For deep partial and full-thickness burns
• Reconstructive surgery: Long-term management of contractures and scarring

Referral Criteria

• Burns centre referral (UK Burns Network): >10% TBSA adult, >5% child/elderly, full thickness >1%, face/hands/feet/genitalia/perineum, inhalational, circumferential, chemical, electrical, associated major trauma

• Baux score: Age + %TBSA = predicted mortality (revised Baux includes inhalation injury)
• Superficial burns: Complete healing without scarring
• Partial thickness: Healing in 2-3 weeks; risk of hypertrophic scarring
• Full thickness: Requires grafting; significant scarring risk
• Inhalational injury: Doubles mortality for any given %TBSA burn
• Electrical burns: Mortality depends on voltage; cardiac arrest and rhabdomyolysis are key risks
• Long-term: Psychological morbidity common - PTSD, depression, anxiety; burns rehabilitation is prolonged

Wallace Rule of Nines (Adult)

Parkland Formula Example

Burns Centre Referral Criteria (UK)

Key Facts

Poisoning is one of the most common reasons for emergency hospital admission in the UK. Most cases are due to intentional self-harm with medications. A systematic approach with ABCDE assessment, toxidrome recognition, and appropriate use of antidotes and decontamination is essential.

Epidemiology

Approximately 170,000 ED attendances for poisoning per year in England. Self-harm by poisoning accounts for approximately 100,000 hospital admissions annually. Paracetamol is the most commonly used agent in self-poisoning (~50% of cases). Approximately 200-300 deaths per year from poisoning in the UK (excluding illicit drugs).

Aetiology

• Intentional self-harm: Most common (~80%) - paracetamol, SSRIs, NSAIDs, opioids
• Recreational drug use: MDMA, cocaine, novel psychoactive substances, opioids
• Accidental: Children (<5 years), elderly (medication errors)
• Environmental: Carbon monoxide, organophosphates

Pathophysiology

Toxicological effects depend on the specific agent, dose, and route. Key mechanisms include:

• Receptor-mediated toxicity: Opioid receptor agonism, anticholinergic receptor blockade
• Enzyme inhibition: Organophosphate cholinesterase inhibition

• Cardiotoxicity: Sodium channel blockade (TCAs), potassium channel effects (sotalol)

Toxidromes

• Anticholinergic: Tachycardia, dry mouth, dilated pupils, urinary retention, confusion, hyperthermia ('dry as a bone, blind as a bat, mad as a hatter')
• Cholinergic: SLUDGE - Salivation, Lacrimation, Urination, Diarrhoea, GI distress, Emesis; miosis, bradycardia, bronchorrhoea
• Sympathomimetic: Tachycardia, hypertension, hyperthermia, dilated pupils, agitation (cocaine, amphetamines)
• Opioid: Miosis, respiratory depression, reduced consciousness, hypotension, bradycardia
• Serotonin syndrome: Clonus, hyperreflexia, hyperthermia, agitation, mydriasis, tremor

Red Flags

• Altered consciousness (GCS <8) - secure airway, consider intubation
• Respiratory depression (RR <12, SpO2 <92%) - naloxone if opioid suspected; ventilatory support
• Cardiovascular compromise - wide QRS (TCAs), arrhythmias, hypotension
• Seizures - particularly with TCAs, tramadol, SSRIs, cocaine
• Hyperthermia >40°C - serotonin syndrome, MDMA, NMS
• Metabolic acidosis - paracetamol (late), methanol, ethylene glycol, salicylates

Bedside

• ABCDE assessment: Priority - secure airway if GCS ≤8
• Blood glucose: Hypoglycaemia (insulin, sulphonylureas) or hyperglycaemia
• ECG: QRS prolongation (TCAs), QTc prolongation (many drugs), arrhythmias
• Temperature: Hyperthermia (serotonin syndrome, NMS, MDMA, sympathomimetics)
• Pupil size: Miosis (opioids, organophosphates) or mydriasis (sympathomimetics, anticholinergics)

Bloods

• Paracetamol level: At 4 hours post-ingestion (or immediately if time unknown) - plot on treatment nomogram
• Salicylate level: If aspirin co-ingestion suspected
• ABG/VBG: pH, lactate, bicarbonate - metabolic acidosis significant
• U&Es, LFTs, coagulation: Organ function assessment
• FBC, glucose: Baseline
• Ethanol level: If alcohol co-ingestion
• Serum osmolality: If toxic alcohol suspected (osmolal gap)

Imaging

• CXR: If aspiration risk or pulmonary oedema
• CT head: If altered consciousness and cause unclear

Special Tests

• Urine drug screen: Limited clinical utility - does not change acute management in most cases
• Specific drug levels: Lithium, digoxin, iron, theophylline, carbamazepine, valproate
• TOXBASE: Consult for all poisoning cases

Non-pharmacological

• ABCDE approach: Secure airway, breathing, circulation first
• Decontamination: Activated charcoal 50g PO (1g/kg in children) if within 1 hour of ingestion of a potentially toxic substance; NOT if airway compromised
• Whole bowel irrigation: Polyethylene glycol - for sustained-release preparations, iron, lithium, body-packers
• Gastric lavage: Rarely indicated - only if life-threatening ingestion within 1 hour and charcoal not effective

Pharmacological

Specific antidotes:

• Paracetamol: N-acetylcysteine (NAC) - 150mg/kg in 200mL 5% glucose over 1h, then 50mg/kg in 500mL over 4h, then 100mg/kg in 1L over 16h
• Opioids: Naloxone 400mcg IV (titrate; may need repeated doses or infusion)
• Benzodiazepines: Flumazenil 200mcg IV (ONLY if pure benzodiazepine OD - risk of seizures with mixed OD)
• TCAs: Sodium bicarbonate 8.4% 50mL IV if QRS >120ms or arrhythmias
• Beta-blockers: Glucagon 2-10mg IV; high-dose insulin-euglycaemia therapy
• Calcium channel blockers: Calcium chloride 10mL 10% IV; high-dose insulin-euglycaemia therapy
• Organophosphates: Atropine 2mg IV doubling every 5 min + pralidoxime 30mg/kg IV
• Digoxin: Digibind (digoxin-specific Fab antibodies)
• Methanol/ethylene glycol: Fomepizole (20mg/kg IV) or ethanol infusion; haemodialysis

Surgical/Interventional

• Haemodialysis/haemofiltration: For salicylates, lithium, methanol, ethylene glycol, theophylline
• Intralipid 20%: For local anaesthetic toxicity, severe lipophilic drug cardiotoxicity

Referral Criteria

• NPIS (0344 892 0111): Complex or unusual poisoning
• ICU: GCS ≤8, haemodynamic instability, respiratory failure
• Psychiatric assessment: ALL intentional overdoses before discharge (NICE CG133)
• Safeguarding: Children with accidental ingestion - assess for neglect/NAI

• Overall mortality from poisoning: <1% with appropriate hospital management
• Paracetamol: Excellent if NAC given within 8 hours; mortality 0.4% with treatment vs ~5% without
• TCA overdose: Mortality ~2-5%; QRS >160ms associated with seizures and arrhythmias
• Opioid overdose: Excellent response to naloxone if given promptly; take-home naloxone programmes reduce community deaths
• Repeated self-harm: ~25% repeat within 1 year; ~3% die by suicide within 10 years

Key Antidotes Summary

Risk Assessment in Intentional Overdose

Key Facts

Paracetamol overdose is the most common cause of acute liver failure and the most frequent reason for calls to the National Poisons Information Service in the UK. Timely treatment with NAC prevents hepatotoxicity in the vast majority of cases.

Epidemiology

Approximately 80,000-100,000 paracetamol overdose presentations to UK EDs annually. ~200 deaths/year from paracetamol poisoning. It is the most common cause of acute liver failure in the UK and USA. ~75% of cases are intentional self-harm; ~25% accidental (therapeutic excess in those taking regular paracetamol for pain).

Aetiology

• Intentional self-harm: Most common - often impulsive, may take multiple medications
• Therapeutic excess (supratherapeutic ingestion): Taking more than recommended dose for pain - often staggered over hours/days; particularly dangerous as nomogram cannot be used
• Accidental: Children accessing medications

Pathophysiology

Paracetamol is normally metabolised in the liver via glucuronidation and sulphation (~95%). A small proportion (~5%) is metabolised by CYP2E1 to the toxic metabolite NAPQI (N-acetyl-p-benzoquinone imine), which is normally detoxified by conjugation with glutathione. In overdose, glutathione is depleted, and NAPQI accumulates causing hepatocellular necrosis (predominantly zone 3 - centrilobular). NAC replenishes glutathione and directly detoxifies NAPQI.

Timeline of Paracetamol Toxicity

Phase 1 (0-24h): Often asymptomatic or mild nausea/vomiting; normal LFTs

Phase 2 (24-72h): Right upper quadrant pain, rising ALT and INR, oliguria

Phase 3 (72-96h): Peak hepatotoxicity - jaundice, coagulopathy, encephalopathy, renal failure, metabolic acidosis, hypoglycaemia. Multi-organ failure in severe cases.

Phase 4 (4-14 days): Recovery phase in survivors - liver regeneration

Risk Factors for Enhanced Toxicity

• Chronic alcohol use (CYP2E1 induction, glutathione depletion)
• Malnutrition, eating disorders (glutathione depletion)
• Enzyme-inducing drugs (carbamazepine, phenytoin, rifampicin)
• HIV infection

Red Flags

• Staggered overdose - cannot use nomogram; treat with NAC if >75mg/kg
• pH <7.3 after resuscitation - indicates severe toxicity (King's criteria)
• INR >3 at 48h or rising beyond 72h - progressive liver failure
• Encephalopathy - grade III/IV indicates need for transplant assessment
• Metabolic acidosis + renal failure + coagulopathy - high mortality without transplant

Bedside

• History: Time of ingestion (CRITICAL), amount taken, preparation (standard vs modified-release), co-ingestions, staggered vs acute
• Observations: Often normal initially

Bloods

• Paracetamol level: At 4 hours post-ingestion (do NOT take before 4h) - plot on treatment nomogram
• ALT: Hepatocellular injury marker - check at presentation and 12-24h
• INR/PT: Coagulation - most sensitive early marker of synthetic liver function
• Creatinine: Renal function
• ABG/VBG: pH - acidosis is a key prognostic indicator
• Venous bicarbonate: Screen for acidosis
• Blood glucose: Hypoglycaemia in severe hepatotoxicity
• Phosphate: Low = good prognosis (liver regeneration); high = poor
• Lactate: Elevated in severe toxicity

Imaging

• Liver USS: If diagnostic uncertainty or suspected chronic liver disease

Special Tests

• Paracetamol-protein adducts: Research tool - can confirm paracetamol toxicity when history unreliable
• TOXBASE: Consult for dosing guidance and nomogram interpretation

Non-pharmacological

• Activated charcoal 50g PO: If within 1 hour of ingestion and airway intact
• Do NOT induce vomiting

Pharmacological

N-Acetylcysteine (NAC) - Modified Prescott Regimen:

• Bag 1: 100mg/kg in 200mL 5% glucose over 1 hour
• Bag 2: 50mg/kg in 500mL 5% glucose over 4 hours
• Bag 3: 100mg/kg in 1000mL 5% glucose over 16 hours
• Total treatment time: 21 hours

Indications for NAC:

• Acute ingestion: Paracetamol level above treatment line on nomogram (single line at 100mg/L at 4h)
• Staggered ingestion (over >1h): NAC if ≥75mg/kg ingested - do NOT use nomogram
• Presentation >8 hours with significant ingestion: Start NAC immediately, do not wait for level
• Clinical features of hepatotoxicity at any stage

NAC anaphylactoid reaction:

• Occurs in ~15-20%, usually within first hour
• Symptoms: Flushing, urticaria, bronchospasm, nausea
• Management: Pause infusion, give chlorphenamine 10mg IV; restart at slower rate once symptoms resolve
• TRUE anaphylaxis to NAC is extremely rare

Post-NAC assessment:

• At end of NAC course: Check ALT, INR, creatinine, paracetamol level
• If ALT rising, INR >1.3, paracetamol still detectable, or clinical concern → continue NAC (bag 3 rate)

Surgical/Interventional

• Liver transplant: For fulminant hepatic failure meeting King's College Criteria
• Referral to specialist hepatology/transplant centre if: pH <7.3, INR >3 at 48h, creatinine >300, encephalopathy, hypoglycaemia

Referral Criteria

• ALT >1000 or rising steeply - hepatology/transplant centre discussion
• INR >3 at 48h or any time rising - transplant centre assessment
• Metabolic acidosis (pH <7.3 after resuscitation) - immediate transplant centre referral
• Encephalopathy - transfer to transplant centre
• ALL intentional overdoses - psychiatric assessment before discharge

• NAC within 8 hours: Hepatotoxicity prevented in >95% of cases; mortality <0.5%
• NAC at 8-24 hours: Reduces severity of hepatotoxicity but does not prevent it entirely
• Without treatment: Mortality ~5-10% overall; higher with staggered overdose
• Fulminant hepatic failure: Mortality ~50% without transplant; ~80% survival with transplant
• King's College Criteria: Identifies patients who will die without transplant with ~90% specificity
• Complete liver recovery: Liver regenerates fully in survivors within 2-4 weeks

Paracetamol Treatment Nomogram

King's College Criteria for Paracetamol-Induced Liver Failure

NAC Infusion Summary (Modified Prescott)

Key Facts

TCA overdose remains one of the most dangerous drug overdoses in the UK despite declining prescription rates. Rapid deterioration can occur, and early recognition of ECG changes is crucial for timely treatment.

Epidemiology

TCA prescriptions have decreased significantly with the rise of SSRIs, but TCAs remain in common use for neuropathic pain, migraine prophylaxis, and nocturnal enuresis. Amitriptyline and dosulepin account for the most toxic overdoses. Dosulepin is the most toxic TCA (highest fatality index).

Aetiology

• Intentional self-harm: Most common - often impulsive
• Accidental overdose: Children, medication errors in elderly
• TCAs prescribed for: Depression, neuropathic pain, migraine, fibromyalgia, IBS, nocturnal enuresis

Pathophysiology

TCAs exert toxicity through multiple mechanisms:

1. Anticholinergic (muscarinic) blockade: Tachycardia, dry mouth, dilated pupils, urinary retention, reduced gut motility
2. Alpha-1 adrenergic blockade: Vasodilation → hypotension
3. Potassium channel blockade: QTc prolongation → torsades de pointes
4. GABA-A receptor antagonism: Lowers seizure threshold
5. Noradrenaline/serotonin reuptake inhibition: Initial sympathetic stimulation

Clinical Features (Dose-Dependent)

Mild toxicity (5-10mg/kg):

• Anticholinergic features: Dry mouth, tachycardia, dilated pupils, drowsiness

Moderate toxicity (10-20mg/kg):

• Confusion, agitation, hallucinations
• Urinary retention, absent bowel sounds
• Sinus tachycardia, mild hypotension
• QRS prolongation beginning

Severe toxicity (>20mg/kg):

• Coma (GCS ≤8)
• Seizures (often generalised)
• QRS >160ms - risk of VT/VF
• Refractory hypotension
• Respiratory depression
• Hyperthermia

Red Flags

• QRS >120ms - administer sodium bicarbonate immediately
• QRS >160ms - high risk of life-threatening arrhythmia
• Seizures - benzodiazepines only (NOT phenytoin - worsens cardiac conduction)
• Rapid GCS deterioration - prepare for intubation
• Right axis deviation of terminal 40ms (R in aVR >3mm) - early sign of sodium channel blockade

Bedside

• 12-lead ECG: CRITICAL - assess QRS duration, QTc, terminal R wave in aVR, axis deviation; repeat every 30 min
• Continuous cardiac monitoring: Minimum 6 hours (some recommend 12h)
• Blood glucose: Exclude hypoglycaemia
• Temperature: Hyperthermia

Bloods

• ABG/VBG: pH (target alkalotic with bicarb); lactate
• Paracetamol level: Always check for co-ingestion
• U&Es: Electrolytes, renal function
• FBC, LFTs: Baseline
• CK: If prolonged seizures or hyperthermia (rhabdomyolysis)

Imaging

• CXR: If aspiration suspected
• CT head: If prolonged seizures or focal neurology

Special Tests

• TCA drug level: NOT routinely available; clinical features and ECG are more useful
• TOXBASE/NPIS: Consult for management guidance

Non-pharmacological

• Resuscitation area: All TCA overdoses - continuous cardiac monitoring
• Activated charcoal 50g PO: If within 1 hour of ingestion and airway protected
• Intubation: If GCS ≤8 or respiratory failure

Pharmacological

Sodium bicarbonate 8.4% IV:

• Indication: QRS >120ms, ventricular arrhythmias, hypotension
• Dose: 50mL (50mmol) IV bolus; repeat until QRS narrows
• Target pH: 7.45-7.55 (alkalosis enhances protein binding of TCA and reverses sodium channel blockade)
• Mechanism: Increases extracellular sodium (overcomes sodium channel blockade) and alkalosis increases drug protein binding

Seizures:

• Diazepam 10-20mg IV or lorazepam 4mg IV
• Do NOT use phenytoin (worsens cardiac conduction)
• Refractory seizures - propofol, thiopental; consider intubation

Hypotension:

• IV crystalloid fluid boluses
• Sodium bicarbonate (if QRS wide)
• Noradrenaline if fluid and bicarb unresponsive
• Avoid vasopressin (worsens arrhythmia risk)

Arrhythmias:

• VT: Sodium bicarbonate first; lidocaine 1mg/kg if refractory
• Do NOT use class Ia/Ic antiarrhythmics, beta-blockers, or calcium channel blockers
• Torsades de pointes: Magnesium 2g IV
• Refractory cardiac arrest: Intralipid 20% (1.5mL/kg bolus, then infusion)

Surgical/Interventional

• ECMO: Last resort for refractory cardiogenic shock
• Intralipid emulsion 20%: For cardiac arrest or refractory cardiovascular collapse

Referral Criteria

• QRS >120ms - resuscitation area, senior review
• Seizures, arrhythmias, or GCS ≤8 - ICU
• Cardiac arrest - full ALS + sodium bicarbonate + intralipid
• All intentional overdoses - psychiatric assessment

• Overall TCA overdose mortality: ~2-5%
• QRS >120ms: ~33% risk of seizures
• QRS >160ms: ~50% risk of ventricular arrhythmias
• If QRS normalises within 6 hours: Very low risk of subsequent arrhythmia
• Survivors: Full recovery expected if no prolonged cardiac arrest or hypoxic brain injury
• Dosulepin: Highest fatality index of all TCAs - 1 week's supply at therapeutic dose can be lethal

TCA ECG Changes (Sequential)

Management Summary

Key Facts

Opioid overdose is a leading cause of preventable death in the UK, particularly from illicit heroin and increasingly from fentanyl. Prompt recognition and naloxone administration are life-saving. Public health approaches including take-home naloxone and supervised consumption facilities are key prevention strategies.

Epidemiology

Opioid-related deaths have increased significantly over the past decade. Approximately 4,500 drug-related deaths per year in the UK (England, Wales, and Scotland combined), with opioids implicated in approximately 50-60%. Scotland has the highest drug death rate in Europe. Risk factors include male sex, social deprivation, periods after release from prison, and loss of tolerance.

Aetiology

• Illicit opioids: Heroin (diamorphine), fentanyl and analogues, methadone diversion
• Prescription opioids: Codeine, tramadol, dihydrocodeine, morphine, oxycodone, fentanyl patches
• OTC opioids: Co-codamol, codeine linctus
• Risk factors for overdose: IV injection, loss of tolerance (post-prison, post-detox), concurrent benzodiazepine/alcohol use, respiratory comorbidity, variable street drug purity

Pathophysiology

Opioids act on mu (μ), kappa (κ), and delta (δ) receptors. Mu-receptor activation in the brainstem depresses the respiratory centre, reducing respiratory rate and tidal volume. Hypoxia and hypercapnia progress to respiratory arrest. Additional effects include central sedation, miosis, reduced gut motility, nausea, histamine release, and hypotension.

Classic Triad

• Respiratory depression: RR <12/min; shallow breathing; apnoea
• Reduced consciousness: Drowsy → unresponsive (GCS ≤8)
• Miosis (pinpoint pupils): Bilateral; may be absent in severe hypoxia (dilated pupils) or mixed overdose

Additional Features

• Cyanosis, hypoxia (SpO2 <92%)
• Hypotension, bradycardia
• Hypothermia
• Track marks, injection sites (IV drug users)
• Pulmonary oedema (non-cardiogenic) - heroin-associated
• Needle still in situ

Red Flags

• RR <8/min or apnoea - immediate naloxone and ventilatory support
• GCS ≤8 - secure airway, recovery position, naloxone
• Fentanyl/carfentanil exposure - may need very high naloxone doses (10mg+)
• Body-packing (swallowed drug packages) - risk of massive release
• Mixed OD (opioid + benzodiazepine) - most common combination in fatal overdose
• Hypothermia - rhabdomyolysis risk from prolonged immobility

Bedside

• ABCDE assessment: Airway and breathing are priority
• SpO2 and respiratory rate: Continuous monitoring
• Blood glucose: Exclude hypoglycaemia
• GCS: Serial assessment
• Temperature: Hypothermia common
• ECG: QTc prolongation (methadone), arrhythmias

Bloods

• ABG/VBG: PaCO2 (elevated = hypoventilation), pH, lactate
• FBC, U&Es, LFTs: Baseline organ function
• CK: Rhabdomyolysis (prolonged immobility on hard surface)
• Paracetamol level: Always check - co-formulated opioids (co-codamol, co-dydramol)

Imaging

• CXR: If aspiration suspected or pulmonary oedema
• Abdominal X-ray/CT: If body-packing suspected

Special Tests

• Urine drug screen: Confirms opioid use but does NOT change acute management
• Naloxone response: Diagnostic and therapeutic - improvement confirms opioid toxicity

Non-pharmacological

• Airway management: Head tilt/chin lift, jaw thrust, recovery position
• Bag-valve-mask ventilation: If inadequate respiratory effort
• Intubation: If naloxone insufficient or prolonged respiratory failure

Pharmacological

Naloxone:

• IV route: 400mcg (0.4mg) IV; repeat every 2-3 min until adequate respiration (up to 10mg or more)
• IM/SC route: 800mcg (0.8mg) IM if no IV access; slower onset (~5 min)
• Intranasal: Nyxoid 1.8mg per nostril - community/pre-hospital
• Titration principle: Aim to restore adequate respiration (RR ≥12) NOT full consciousness - avoids precipitating severe withdrawal
• Naloxone infusion: Two-thirds of initial effective dose per hour in 5% glucose - for long-acting opioids (methadone, sustained-release preparations)

Monitoring post-naloxone:

• Observe minimum 2 hours after last naloxone dose for short-acting opioids
• Observe 6-12 hours (or longer) for methadone/sustained-release opioid overdose
• Watch for re-narcotisation when naloxone wears off

Surgical/Interventional

• Whole bowel irrigation: For body-packers (polyethylene glycol)
• Surgical retrieval: If body-packer with clinical toxicity or package rupture

Referral Criteria

• All overdoses - psychiatric assessment if intentional
• Drug and alcohol services - referral for opioid dependence (opiate substitution therapy)
• Take-home naloxone - provide to patient and family at discharge
• Safeguarding - children in household of opioid users

• With prompt naloxone: Excellent - full recovery expected in uncomplicated cases

• Complications: Aspiration pneumonia, non-cardiogenic pulmonary oedema, rhabdomyolysis (from immobility), anoxic brain injury (from prolonged hypoxia)
• Post-prison release: 7-8× increased risk of opioid death in first 2 weeks (loss of tolerance)
• Naloxone take-home programmes: Reduce opioid-related deaths by ~30-50% in target populations

Naloxone Dosing Guide

Observation Times Post-Naloxone

Take-Home Naloxone (UK)

Key Facts

Alcohol intoxication and its complications represent a major burden on UK emergency services. The key challenge is not managing intoxication itself but identifying and treating co-existing or mimicking conditions that may be masked by alcohol.

Epidemiology

Alcohol-related hospital admissions in England exceed 1 million per year. ED attendances related to alcohol account for approximately 12-15% of all presentations (higher at weekends and overnight). Alcohol-related deaths in the UK: approximately 10,000 per year. Alcohol misuse costs the NHS approximately £3.5 billion annually.

Aetiology

• Acute intoxication: Binge drinking, chronic heavy drinking
• Alcohol use disorder: Affects approximately 6% of adults in England
• High-risk groups: Young adults (binge drinking), homeless populations, those with mental health comorbidity

Pathophysiology

Ethanol is a CNS depressant acting primarily via GABA-A receptor potentiation and NMDA receptor inhibition. It causes dose-dependent sedation, impaired coordination, slurred speech, and at high doses, respiratory depression and coma. Chronic use leads to neuroadaptation (GABA downregulation, NMDA upregulation), explaining tolerance and the potentially life-threatening withdrawal syndrome when alcohol is ceased.

Stages of Intoxication

• Mild (50-150mg/dL): Disinhibition, impaired judgement, slurred speech
• Moderate (150-250mg/dL): Ataxia, dysarthria, emotional lability, nausea/vomiting
• Severe (250-400mg/dL): Stupor, marked ataxia, hypothermia, risk of aspiration
• Potentially fatal (>400mg/dL): Coma, respiratory depression, cardiovascular collapse

Red Flags

• Reduced GCS not proportionate to estimated alcohol intake - consider head injury, co-ingestion, metabolic cause
• Focal neurological signs - CT head to exclude intracranial pathology
• Hypoglycaemia - common in chronic drinkers and malnourished patients
• Hypothermia - particularly outdoor exposure while intoxicated
• Persistent vomiting - risk of Mallory-Weiss tear, aspiration, Boerhaave syndrome
• Confusion disproportionate to alcohol level - Wernicke's encephalopathy

Bedside

• ABCDE assessment: Airway protection is priority
• Blood glucose: Immediately - treat hypoglycaemia
• GCS: Serial monitoring - should improve over time; if not, investigate further
• Temperature: Hypothermia risk
• ECG: Arrhythmias (holiday heart syndrome - AF)

Bloods

• Blood alcohol level: Confirms intoxication; correlate with clinical state
• Blood glucose: Hypoglycaemia (impaired gluconeogenesis)
• U&Es: Electrolyte disturbance (hyponatraemia, hypokalaemia, hypomagnesaemia)
• LFTs: Acute/chronic liver damage
• FBC: Macrocytosis (chronic alcohol use), thrombocytopenia
• Paracetamol level: Always check for co-ingestion
• VBG/ABG: Lactate, pH, ketones
• Amylase/lipase: If abdominal pain (pancreatitis)

Imaging

• CT head: If head injury suspected, focal neurology, GCS not improving, anticoagulated

Special Tests

• AUDIT score: Alcohol Use Disorders Identification Test - screen before discharge
• Serum magnesium: Often low in chronic alcohol use

Non-pharmacological

• Airway protection: Recovery position if unable to maintain airway; intubation if GCS ≤8 with no improvement
• Observation: Safe, monitored environment; serial GCS
• Rehydration: IV fluids (0.9% NaCl or Hartmann's) if dehydrated
• Warming: If hypothermic
• Brief intervention: For hazardous/harmful drinking - evidence-based approach at discharge

Pharmacological

• IV glucose: 100mL 20% glucose if hypoglycaemic - but give IV Pabrinex FIRST if Wernicke's suspected
• IV Pabrinex (high-potency B vitamins including thiamine): Pairs 1+2 TDS for 3-5 days if malnourished, suspected Wernicke's, or chronic alcohol use - BEFORE glucose administration
• Antiemetics: Ondansetron 4mg IV if significant vomiting
• Alcohol withdrawal management (if developing):
  • Chlordiazepoxide reducing regimen (e.g., 30mg QDS day 1, reducing over 5-7 days) - guided by CIWA-Ar score
  • Symptom-triggered dosing is safer than fixed-dose regimens
  • Pabrinex throughout withdrawal period

Surgical/Interventional

• Not usually required; manage complications as they arise

Referral Criteria

• AUDIT score ≥8: Brief intervention; ≥16: Referral to alcohol services
• Dependent drinking: Alcohol liaison nurse, community alcohol team
• Recurrent presentations: Safeguarding, social services, dual diagnosis team if mental health comorbidity
• All deliberate self-harm with alcohol: Psychiatric assessment

• Acute intoxication: Self-limiting if uncomplicated; death from aspiration, respiratory depression, or hypothermia is preventable
• Alcohol-related liver disease: Leading cause of liver disease in the UK; ~6,000 deaths/year
• Alcohol withdrawal: Mortality from delirium tremens ~5% if untreated, <1% with treatment
• Brief interventions: NNT 8 to reduce hazardous drinking by 1 person
• Wernicke's encephalopathy: If untreated → 80% develop Korsakoff's syndrome (irreversible amnesia)

CIWA-Ar Score Components

Score >8: Treat; >15: Moderate withdrawal; >20: Severe withdrawal.

Alcohol Withdrawal Timeline

Key Facts

Recreational drug intoxication presents an evolving challenge with the emergence of novel psychoactive substances and changing patterns of drug use. Management is predominantly supportive with treatment of specific complications.

Epidemiology

Drug-related deaths in the UK exceed 4,500 per year and are increasing. Opioids remain the leading cause of drug death. Cocaine-related deaths have tripled over the past decade. NPS-related deaths are increasing. Scotland has the highest drug death rate in Europe.

Aetiology

• Stimulants: Cocaine, amphetamines, MDMA, methamphetamine, mephedrone
• Depressants: GHB/GBL, benzodiazepines (recreational), ketamine
• Cannabis and synthetic cannabinoids: 'Spice', K2
• Hallucinogens: LSD, psilocybin, DMT
• Dissociatives: Ketamine, PCP, nitrous oxide
• Novel psychoactive substances: Evolving range of synthetic drugs

Pathophysiology

Different drugs act on different neurotransmitter systems:

• Stimulants: Increase catecholamines (dopamine, noradrenaline) → sympathomimetic toxidrome
• MDMA: Serotonin and noradrenaline release → serotonergic syndrome, hyperthermia, SIADH
• GHB/GBL: GABA-B agonism → rapid-onset sedation
• Synthetic cannabinoids: Full CB1 agonism (unlike THC partial agonism) → unpredictable severe effects

Stimulant Toxidrome (Cocaine, Amphetamines, MDMA)

• Agitation, psychosis, paranoia
• Tachycardia, hypertension, hyperthermia
• Dilated pupils (mydriasis)
• Seizures, arrhythmias, MI (cocaine), rhabdomyolysis

MDMA-Specific

• Hyponatraemia (dilutional - excess water drinking)
• Serotonin syndrome (clonus, hyperreflexia, hyperthermia)
• Hepatotoxicity

GHB/GBL

• Rapid deep sedation → coma (onset 15-30 min, duration 2-4h)
• Bradycardia, respiratory depression
• Agitated emergence from coma

Synthetic Cannabinoids

• Agitation, psychosis, seizures (unlike natural cannabis)
• Tachycardia, AKI, rhabdomyolysis

Red Flags

• Hyperthermia >40°C - actively cool (MDMA, cocaine, serotonin syndrome)
• Chest pain in cocaine user - ACS; treat with benzodiazepines, GTN, avoid beta-blockers
• Seizures - benzodiazepines first-line
• Hyponatraemia (Na⁺ <120) - hypertonic saline if symptomatic
• Body-packing - risk of massive drug release

Bedside

• ABCDE assessment: Priority
• Temperature: Hyperthermia is a medical emergency
• Blood glucose: Exclude hypoglycaemia
• ECG: Arrhythmias, QTc prolongation, Brugada-like (cocaine)
• GCS: Serial monitoring

Bloods

• U&Es: Sodium (MDMA - hyponatraemia), potassium, creatinine (AKI)
• CK: Rhabdomyolysis (stimulants, prolonged seizures, hyperthermia)
• Troponin: If chest pain (cocaine-associated MI)
• LFTs: Hepatotoxicity (MDMA, cocaine)
• ABG/VBG: pH, lactate
• Coagulation: DIC in severe hyperthermia
• Paracetamol level: Always check for co-ingestion

Imaging

• CXR: If respiratory symptoms
• CT head: If seizures, focal neurology, prolonged altered consciousness
• Abdominal X-ray/CT: If body-packing suspected

Special Tests

• Urine drug screen: Confirmatory but rarely changes acute management
• TOXBASE/NPIS: For NPS identification and management guidance

Non-pharmacological

• Supportive care: ABCDE, calm environment, reassurance (for mild stimulant intoxication)
• Active cooling: For hyperthermia >39°C - remove clothing, cold IV fluids, ice packs, evaporative cooling; consider dantrolene if >41°C
• Fluid restriction: For MDMA-induced hyponatraemia (NOT IV fluids)

Pharmacological

Stimulant toxicity (cocaine/amphetamines):

• Benzodiazepines (diazepam 10-20mg IV) for agitation, hypertension, tachycardia
• GTN for cocaine-associated chest pain
• Avoid beta-blockers in cocaine toxicity (risk of unopposed alpha stimulation)
• Sodium bicarbonate if wide QRS on ECG

MDMA toxicity:

• Cooling measures
• Benzodiazepines for seizures/agitation
• Cyproheptadine 12mg PO for serotonin syndrome (then 4mg every 2h)
• Hypertonic saline 3% (100mL over 10 min) if Na⁺ <120 with seizures/severe symptoms

GHB/GBL:

• Supportive - airway protection; usually self-limiting
• Atropine if symptomatic bradycardia
• Do NOT use flumazenil (not effective)

Ketamine:

• Benzodiazepines for emergence reactions/agitation
• Monitoring of cardiovascular parameters

Surgical/Interventional

• Body-packer: Whole bowel irrigation; surgical retrieval if package rupture with clinical toxicity

Referral Criteria

• ICU: Hyperthermia >40°C, cardiovascular instability, refractory seizures, severe hyponatraemia
• Drug and alcohol services: All patients with recreational drug use
• Psychiatric: If self-harm or suicidal ideation
• Safeguarding: If children exposed to drug use in the home

• Cocaine-associated MI: 5-10% mortality if not recognised; excellent outcome with appropriate management
• MDMA fatalities: Primarily from hyperthermia, hyponatraemia, or serotonin syndrome
• GHB/GBL: Narrow therapeutic window; death from respiratory depression; usually recover fully if airway managed
• Synthetic cannabinoids: Increasing mortality and morbidity; unpredictable pharmacology

Drug-Specific Emergency Management Summary

Serotonin Syndrome Diagnostic Criteria (Hunter)

Key Facts

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS) are the two major hyperglycaemic emergencies. Both are potentially fatal without treatment. DKA predominantly affects type 1 diabetes (but can occur in type 2), while HHS occurs in type 2 diabetes.

Epidemiology

DKA accounts for approximately 8,000-10,000 admissions per year in England. In-hospital mortality for DKA is approximately 0.5-2% (higher in elderly and those with significant comorbidity). HHS has a higher mortality of approximately 15-20% despite being less common. DKA is the most common cause of death in young people with type 1 diabetes.

Aetiology

DKA triggers:

• Infection (most common precipitant ~40%)
• Non-adherence to insulin (especially in young people)
• New diagnosis of type 1 diabetes
• Acute illness, surgery, trauma
• Drugs: Corticosteroids, SGLT2 inhibitors (can cause euglycaemic DKA)

HHS triggers:

• Infection (most common)
• MI, stroke
• Non-adherence to medications
• New diagnosis of type 2 diabetes

Pathophysiology

DKA Presentation

• Polyuria, polydipsia, weight loss
• Nausea, vomiting, abdominal pain (may mimic surgical abdomen)
• Kussmaul breathing (deep, sighing respirations - compensatory for acidosis)
• Ketotic breath (pear drops/acetone smell)
• Dehydration (dry mucous membranes, reduced skin turgor, tachycardia)
• Altered consciousness (10-15% present with GCS <12)

HHS Presentation

• Insidious onset over days to weeks
• Profound dehydration (often more severe than DKA)
• Altered consciousness, confusion, drowsiness, coma
• Focal neurological signs (may mimic stroke)
• NO significant ketoacidosis
• Often elderly with multiple comorbidities

Red Flags

• pH <7.1 - severe DKA, requires critical care
• Potassium <3.5 or >6.0 - life-threatening; correct before/during insulin therapy
• Osmolality >350 - severe HHS; high mortality
• New confusion or GCS deterioration in DKA - cerebral oedema (especially children)
• Euglycaemic DKA (glucose <14 with ketoacidosis) - SGLT2 inhibitor use

Bedside

• Capillary blood glucose: Immediately
• Capillary/blood ketones: β-hydroxybutyrate - >3 mmol/L diagnostic for DKA
• VBG/ABG: pH, bicarbonate, lactate, potassium
• Urine dipstick: Ketonuria, UTI
• ECG: Hyperkalaemia/hypokalaemia changes
• Weight: For insulin infusion calculation

Bloods

• U&Es: Potassium (CRITICAL - guide replacement), sodium (corrected), creatinine, urea
• FBC: WCC (infection trigger - note WCC may be elevated in DKA without infection)
• CRP: If infection suspected
• Serum osmolality: Calculated: 2(Na⁺) + glucose + urea (all in mmol/L) - >320 = HHS
• Blood cultures: If febrile
• HbA1c: If new diagnosis
• Amylase/lipase: May be elevated in DKA (not always pancreatitis)

Imaging

• CXR: If pneumonia suspected as trigger
• CT head: If focal neurology in HHS (exclude stroke)

Special Tests

• Hourly capillary glucose and ketones: Guide insulin adjustment
• VBG at 1h, 2h, 4h, 6h, 12h, 24h: Monitor resolution

DKA Management (JBDS Protocol)

Fluid resuscitation:

• 0.9% NaCl: 1L over 1h, 1L over 2h, 1L over 2h, 1L over 4h, 1L over 4h, 1L over 6h
• Switch to 10% glucose (125mL/hr) when glucose <14 mmol/L (continue insulin to clear ketones)

Fixed-rate insulin infusion (FRII):

• 0.1 units/kg/hr (e.g., 7 units/hr for 70kg patient)
• Continue patient's background long-acting insulin (prevent rebound DKA)
• Do NOT bolus insulin

Potassium replacement:

• K⁺ >5.5: No potassium added
• K⁺ 3.5-5.5: 40mmol KCl per litre of fluid
• K⁺ <3.5: Senior review; aggressive replacement before insulin

Resolution targets (within first 24h):

• Ketones falling by ≥0.5 mmol/L/hr
• Bicarbonate rising by ≥3 mmol/L/hr
• Glucose falling by ≥3 mmol/L/hr
• If not achieving targets → increase FRII by 1 unit/hr

HHS Management (JBDS Protocol)

• Cautious rehydration: 0.9% NaCl - aim to replace 50% of estimated fluid deficit in first 12h, remainder over next 12-24h
• Insulin: Only start if ketones >1 mmol/L or glucose not falling with fluids alone; low rate 0.05 units/kg/hr
• Aim: Glucose fall ≤5 mmol/L/hr; osmolality fall ≤3-8 mOsm/kg/hr (too rapid correction risks osmotic demyelination and cerebral oedema)
• VTE prophylaxis: LMWH - high thromboembolic risk
• Potassium replacement: As per DKA protocol

Referral Criteria

• Severe DKA (pH <7.1, K⁺ <3.5, GCS <12) - critical care
• HHS - HDU/critical care recommended
• Children with DKA - paediatric protocol; cerebral oedema risk
• New diagnosis diabetes - diabetes specialist nurse and endocrinology review
• Recurrent DKA - diabetes psychology review for adherence support

• DKA mortality: ~0.5-2% (higher in elderly and those with comorbidity)
• HHS mortality: ~15-20% (largely due to older age, comorbidity, and thrombotic complications)
• Cerebral oedema (paediatric DKA): ~1% incidence; ~25% mortality; risk factors include young age, new diagnosis, excessive fluid rate, rapid glucose fall
• Recurrent DKA: Strong predictor of future complications and premature mortality in type 1 diabetes
• Post-discharge: All patients need diabetes specialist review within 24-48h; insulin dose optimisation

DKA vs HHS Comparison

JBDS DKA Treatment Targets

Key Facts

Adrenal crisis is an under-recognised emergency that carries significant mortality if not treated promptly. It should be considered in any patient with unexplained hypotension, particularly those with a history of steroid use or known adrenal insufficiency.

Epidemiology

Primary adrenal insufficiency (Addison's disease) has a prevalence of approximately 100-140 per million in the UK. However, adrenal crisis due to secondary causes (chronic steroid therapy, pituitary disease) is far more common. Approximately 5-10 crises per 100 patient-years occur in those with known adrenal insufficiency. Adrenal crisis is the cause of death in approximately 6-15% of patients with Addison's disease.

Aetiology

Primary adrenal insufficiency:

• Autoimmune adrenalitis (Addison's disease) - 80% in UK; may be part of autoimmune polyendocrine syndrome
• TB - most common cause worldwide
• Adrenal haemorrhage (Waterhouse-Friderichsen syndrome - meningococcal sepsis)
• Metastases, infiltration (lymphoma, amyloid)

Secondary adrenal insufficiency (most common overall):

• Chronic corticosteroid therapy (>5mg prednisolone >3 weeks) - HPA axis suppression
• Pituitary disease (tumour, surgery, apoplexy, Sheehan's syndrome)

Pathophysiology

Cortisol is essential for maintaining vascular tone, gluconeogenesis, and the stress response. In adrenal insufficiency, the adrenal glands cannot produce adequate cortisol. During physiological stress (infection, surgery, trauma), cortisol requirements increase dramatically. Without this cortisol surge, cardiovascular collapse occurs. In primary disease, aldosterone deficiency also contributes (hyponatraemia, hyperkalaemia, dehydration).

Acute Presentation

• Severe hypotension (refractory to fluids/vasopressors until steroids given)
• Shock, tachycardia, peripheral vasoconstriction
• Nausea, vomiting, abdominal pain (may mimic acute abdomen)
• Confusion, reduced consciousness
• Fever (may be triggered by intercurrent infection)

Chronic Features (May Be Present)

• Hyperpigmentation (primary only - ACTH-driven; buccal mucosa, skin creases, scars)
• Weight loss, fatigue, anorexia
• Postural hypotension
• Salt craving (aldosterone deficiency)

Red Flags

• Hypotension not responding to fluids - give IV hydrocortisone
• Patient on long-term steroids presenting with acute illness - stress dose required
• Hyponatraemia + hyperkalaemia + hypoglycaemia - classic triad
• Post-surgical patient on chronic steroids who becomes hypotensive - adrenal crisis until proven otherwise

Bedside

• Blood glucose: Hypoglycaemia (impaired gluconeogenesis)
• Blood pressure: Severe hypotension
• ECG: Hyperkalaemia changes (peaked T waves, wide QRS)
• Temperature: Hypothermia or fever (infection trigger)

Bloods

• Random cortisol: Take BEFORE giving hydrocortisone if possible (but do NOT delay treatment) - cortisol <100 nmol/L in acute illness is diagnostic; <300 is suspicious
• ACTH: Elevated in primary (>100 pg/mL), low/normal in secondary
• U&Es: Hyponatraemia, hyperkalaemia, raised urea
• Blood glucose: Hypoglycaemia
• FBC: Eosinophilia (cortisol normally suppresses eosinophils)
• TFTs: Coexisting hypothyroidism (autoimmune polyendocrine syndrome)
• Calcium: Hypercalcaemia may occur

Imaging

• CT adrenals: Haemorrhage, calcification (TB), metastases
• MRI pituitary: If secondary cause suspected

Special Tests

• Short Synacthen test: Definitive test for adrenal insufficiency - measure cortisol at 0 and 30 min after 250mcg tetracosactide IV; cortisol <550 nmol/L at 30 min = adrenal insufficiency
• Adrenal autoantibodies (21-hydroxylase): For autoimmune Addison's

Non-pharmacological

• Do NOT delay treatment for investigations - adrenal crisis is a clinical diagnosis
• IV access: Immediately

Pharmacological

Acute treatment:

• Hydrocortisone 100mg IV immediately (or IM if no IV access)
• 0.9% NaCl: 1L rapid bolus, then guided by clinical response and electrolytes
• 50% glucose IV: If hypoglycaemic (50mL)
• Continue hydrocortisone 50mg IV/IM 6-hourly until stable (usually 24-48h)
• Then convert to oral hydrocortisone (20mg morning, 10mg afternoon) and titrate
• If primary adrenal insufficiency - add fludrocortisone 50-200mcg OD when oral intake established (not needed acutely as high-dose hydrocortisone has mineralocorticoid activity)

Hyperkalaemia management (if K⁺ >6.0):

• Calcium gluconate 10% 30mL IV (cardioprotection)
• Insulin 10 units + 25g glucose IV
• Salbutamol 10mg nebulised
• Hydrocortisone will also help (promotes renal K⁺ excretion)

Treat precipitant:

• Antibiotics if infection suspected
• Investigate and treat underlying trigger

Referral Criteria

• All adrenal crises - endocrinology review
• New diagnosis - investigation for cause (Synacthen test, ACTH, adrenal antibodies)
• Patient education - sick day rules, emergency injection technique, MedicAlert, steroid card

• With prompt treatment: Rapid recovery expected; most patients stabilise within hours
• Without treatment: Fatal - cardiovascular collapse
• Mortality from adrenal crisis: ~0.5% per crisis episode; ~6-15% of Addison's patients die from adrenal crisis over their lifetime
• Prevention: Patient education (sick day rules), steroid emergency card, MedicAlert bracelet, IM hydrocortisone kit
• Long-term: Lifelong replacement required for primary adrenal insufficiency; regular endocrine follow-up

Sick Day Rules for Adrenal Insufficiency

Steroid Replacement in Adrenal Insufficiency

Key Facts

AKI is extremely common and carries significant mortality. It is often preventable and early recognition with appropriate management can reverse most cases. The key is to identify the cause (pre-renal, intrinsic, or post-renal), stop nephrotoxins, and treat urgently.

Epidemiology

AKI affects 13-18% of hospitalised patients and is increasing in incidence. Community-acquired AKI accounts for ~50% of cases. In-hospital mortality: Stage 1 ~10%; Stage 2 ~20%; Stage 3 ~25-30%. AKI is associated with increased length of stay, ICU admission, and progression to CKD.

Aetiology

Pre-renal (55%):

• Hypovolaemia: Dehydration, haemorrhage, burns
• Hypotension: Sepsis, cardiogenic shock
• Drugs: ACEi/ARB, NSAIDs (reduce GFR)

Intrinsic renal (35%):

• Acute tubular necrosis (ATN): Ischaemic (prolonged pre-renal) or nephrotoxic (aminoglycosides, contrast, myoglobin)
• Glomerulonephritis: ANCA vasculitis, anti-GBM, lupus nephritis
• Acute interstitial nephritis: Drug-induced (penicillins, NSAIDs, PPIs)
• Rhabdomyolysis: Crush injury, statins, seizures, heat stroke

Post-renal (10%):

• Ureteric obstruction: Stones, tumour, retroperitoneal fibrosis
• Bladder outflow obstruction: BPH, prostate cancer, urethral stricture

Pathophysiology

Pre-renal AKI results from reduced renal perfusion. If sustained, it progresses to ATN (intrinsic). ATN involves necrosis of tubular epithelial cells from ischaemia or direct toxicity, leading to loss of concentration ability, impaired sodium reabsorption, and cast formation. Post-renal AKI results from increased hydrostatic pressure proximal to obstruction, impairing glomerular filtration.

Clinical Features

• Often asymptomatic - detected on blood tests (AKI e-alert)
• Reduced urine output (<0.5mL/kg/hr for >6h)
• Fluid overload: Peripheral oedema, pulmonary oedema, raised JVP
• Uraemia: Nausea, vomiting, confusion, pruritus, pericarditis
• Features of underlying cause: Fever (infection), rash (vasculitis), loin pain (obstruction)

Red Flags

• Anuria - complete obstruction or severe intrinsic disease
• Hyperkalaemia >6.0 mmol/L - life-threatening arrhythmia risk
• Pulmonary oedema - urgent diuresis or dialysis
• Uraemic encephalopathy/pericarditis - emergency dialysis indication
• Active urinary sediment (red cell casts, protein) - suggests glomerulonephritis; urgent nephrology input

Bedside

• Urine output: Catheterise - measure hourly; <0.5mL/kg/hr is significant
• Fluid status: JVP, peripheral oedema, lung crackles, blood pressure
• Bladder scan: Post-void residual - exclude urinary retention
• Urine dipstick: Blood + protein = glomerular disease; leucocytes/nitrites = infection
• ECG: Hyperkalaemia changes (peaked T waves, wide QRS, sine wave)

Bloods

• U&Es: Creatinine (serial), potassium, sodium, urea
• FBC: Anaemia (CKD, HUS), eosinophilia (interstitial nephritis)
• CRP: Infection/inflammation
• CK: Rhabdomyolysis (>5× ULN)
• LDH, reticulocytes, haptoglobin, blood film: If haemolytic uraemic syndrome (HUS/TTP) suspected
• Immunology: ANCA, anti-GBM, ANA, complement (C3/C4) - if glomerulonephritis suspected

Imaging

• Renal USS: Within 6 hours if obstruction suspected (hydronephrosis), within 24h for all AKI

Special Tests

• Urine sodium and osmolality: Pre-renal (Na⁺ <20, osmolality >500) vs ATN (Na⁺ >40, osmolality <350)
• Urine protein:creatinine ratio (uPCR): Quantify proteinuria
• Renal biopsy: If intrinsic cause unclear and diagnosis would change management

Non-pharmacological

• Stop nephrotoxins: 'Hold the DAMN drugs' - Diuretics (if hypovolaemic), ACEi/ARB, Metformin, NSAIDs; also aminoglycosides, contrast
• Catheterise: Monitor urine output; relieve retention if post-renal
• Daily U&Es: Track trajectory

Pharmacological

• IV fluid resuscitation: 250-500mL 0.9% NaCl bolus if hypovolaemic; reassess response
• Hyperkalaemia management (if K⁺ >6.0):
  • Calcium gluconate 10% 30mL IV (cardiac membrane stabilisation)
  • Insulin 10 units + 25g glucose IV (shift K⁺ intracellularly)
  • Salbutamol 10-20mg nebulised
  • Calcium resonium 15g PO/PR (slow K⁺ removal)
  • Sodium bicarbonate 8.4% 50mL if acidotic
• IV furosemide: 40-250mg for fluid overload (only if not hypovolaemic)
• Treat underlying cause: Antibiotics for sepsis, hydration for rhabdomyolysis (target UO >200mL/hr)

Surgical/Interventional

• Nephrostomy or ureteric stent: For obstructive uropathy
• Catheter insertion: For bladder outflow obstruction
• Renal replacement therapy (dialysis): For refractory hyperkalaemia, acidosis, fluid overload, uraemic complications, certain toxins (AEIOU)

Referral Criteria

• AKI stage 3 - nephrology referral
• Suspected glomerulonephritis/vasculitis - urgent nephrology
• Obstruction requiring intervention - urology
• Indications for dialysis - renal/ICU team
• AKI with unknown cause - nephrology input within 24h

• Pre-renal AKI: Usually reversible within 24-48h with appropriate fluid management
• ATN: Recovery typically over 1-3 weeks; some progress to CKD
• Post-renal: Excellent recovery if obstruction relieved promptly (within 48h)
• Hospital mortality: Stage 1 ~10%, Stage 2 ~20%, Stage 3 ~25-30%
• CKD progression: ~20% of AKI survivors develop CKD within 5 years; ~5% require long-term dialysis
• Post-obstructive diuresis: Can cause severe polyuria - monitor and replace fluids

KDIGO AKI Staging

Indications for Emergency Dialysis (AEIOU)