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What an Emergency Medicine Duty Doctor Must Know

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1. THE CORE MINDSET: STABILIZE, THEN DIAGNOSE

• Primary survey first (ABCDE)
• Identify and treat immediately life-threatening conditions in real time
• Only then move to history, secondary exam, and investigations

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2. AIRWAY MANAGEMENT - Top Priority

• GCS ≤ 8, or inability to protect airway
• Hypoxia refractory to oxygen (SpO₂ < 90% on high-flow O₂)
• Respiratory failure (RR > 35 or < 6, accessory muscle use, exhaustion)
• Anticipated deterioration (burns to airway, anaphylaxis, neck trauma)

• Cervical spine injuries above C3 cause rapid respiratory paralysis - intubate early
• Propofol is preferred for post-intubation sedation when hypotension is NOT a concern
• Retropharyngeal hematoma, maxillofacial trauma = predicted difficult airway - have surgical airway backup ready
• Confirm placement: waveform capnography (gold standard), bilateral chest auscultation, CXR

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3. SHOCK - Recognition & Management

1. Large-bore IV x2 + IO if failed
2. Fluid challenge: 30 mL/kg crystalloid (NS or LR) rapidly
3. Vasopressors if MAP < 65 despite fluids: Norepinephrine first-line (start 0.05 mcg/kg/min, titrate up)
4. Identify and treat underlying cause

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4. SEPSIS - The 1-Hour Bundle (Surviving Sepsis Campaign 2021)

1. Measure lactate - if > 2 mmol/L, recheck in 2-4 hours; if > 4 mmol/L = high risk
2. Blood cultures x2 (aerobic + anaerobic) - BEFORE antibiotics
3. Broad-spectrum antibiotics - within 1 hour (do not delay for cultures)
4. 30 mL/kg IV crystalloid if hypotensive OR lactate > 4 mmol/L
5. Vasopressors if MAP < 65 despite fluids: Norepinephrine, add vasopressin for support

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5. CARDIAC ARREST - ACLS Framework

• CPR quality: 100-120 compressions/min, 5-6 cm depth, full recoil, minimize interruptions
• Defibrillation for shockable rhythms (VF/pVT) within 3 minutes
• Epinephrine 1 mg IV every 3-5 minutes
• Amiodarone 300 mg IV for refractory VF/pVT

• Target SpO₂ 94-98%, PaCO₂ 35-45 mmHg
• MAP ≥ 65 mmHg
• Targeted Temperature Management (TTM): avoid fever (≥37.7°C is harmful)
• 12-lead ECG immediately - cath lab activation if STEMI

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6. TRIAGE - Emergency Severity Index (ESI)

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7. CRITICAL PRESENTATIONS TO RECOGNIZE IMMEDIATELY

A. Acute Coronary Syndrome

• 12-lead ECG within 10 minutes of arrival
• STEMI: ST elevation ≥ 1 mm in ≥2 contiguous limb leads or ≥ 2 mm in precordial leads
• Goal: door-to-balloon < 90 minutes
• NSTEMI/UA: Aspirin 325 mg + heparin + risk-stratify (TIMI/GRACE score)

B. Stroke

• FAST: Face drooping, Arm weakness, Speech difficulty, Time to call
• Door-to-CT < 25 minutes
• tPA (alteplase) if: ischemic stroke + onset < 4.5 hours + no contraindications
• Thrombectomy if large vessel occlusion + onset < 24 hours
• Keep BP < 185/110 before tPA; < 180/105 after
• Do NOT lower BP aggressively in ischemic stroke (risks penumbra infarction)

C. Acute Pulmonary Edema

• Upright position, high-flow O₂
• IV furosemide 40-80 mg
• IV nitrates (GTN) if BP > 90 systolic
• CPAP/BiPAP reduces intubation rate significantly
• Avoid fluid boluses

D. Anaphylaxis

• Epinephrine 0.5 mg IM (anterolateral thigh) - FIRST line, no delay
• Repeat every 5-15 min if needed
• IV access + fluids + antihistamines + steroids as adjuncts
• Observe minimum 4-6 hours; 24 hours if biphasic reaction risk

E. Tension Pneumothorax

• Clinical diagnosis: respiratory distress + hypoxia + absent breath sounds + tracheal deviation + hypotension
• Do NOT wait for CXR - needle decompression immediately
• 2nd intercostal space, midclavicular line, 14G needle
• Followed by chest drain (5th ICS, midaxillary line)

F. Aortic Dissection

• Tearing/ripping chest pain radiating to back, unequal BP in arms
• CT Angiography chest (widened mediastinum on CXR is a clue)
• Type A (ascending): emergency surgery
• Type B (descending): BP control (target systolic 100-120) - labetalol or esmolol

G. Pulmonary Embolism (massive)

• Hemodynamic instability + suspected PE = systemic thrombolysis (alteplase 100 mg over 2 hrs)
• If thrombolysis contraindicated: surgical embolectomy or catheter-directed therapy
• Wells score + D-dimer for stratification in stable patients

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8. TOXICOLOGY ESSENTIALS

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9. PROCEDURAL SKILLS - Must Be Proficient

• RSI and endotracheal intubation - including surgical airway (cricothyrotomy)
• Central venous access (IJV, subclavian, femoral) and arterial line
• Intraosseous (IO) access - 80-90 seconds; any resuscitation drug can go through IO
• Chest drain/thoracostomy - tension PTX, hemothorax
• Pericardiocentesis - cardiac tamponade
• DC cardioversion - for unstable arrhythmias
• Transcutaneous pacing - symptomatic bradycardia
• Focused POCUS - FAST exam (trauma), cardiac (tamponade, LV function, IVC), lung (PTX, pulmonary edema), DVT

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10. ECG INTERPRETATION - High-Yield

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11. PAIN & SEDATION IN THE ED

• Procedural sedation: Ketamine (1-2 mg/kg IV, 4 mg/kg IM) - preserves airway reflexes, safe in most situations
• Ketamine is analgesic, amnestic, and bronchodilatory - excellent for asthma + painful procedures
• Multimodal analgesia: Paracetamol + NSAID + opioid (stepwise)
• Opioids: Morphine 0.1 mg/kg IV or Fentanyl 1-2 mcg/kg IV (faster onset, less histamine release)

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12. PEDIATRIC EM PEARLS

• Broselow tape for weight estimation and drug dosing
• Normal RR in infants: 40-60/min; normal HR in neonates: 120-160/min
• Febrile neonate < 28 days: full septic workup + empirical antibiotics (ampicillin + gentamicin)
• IO access is first-line in pediatric arrest if IV fails within 60-90 seconds
• Fluid boluses in pediatric sepsis: 10-20 mL/kg (not 30 mL/kg as in adults)
• Pediatric resuscitation drugs use weight-based dosing - always double-check

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13. DISPOSITION DECISIONS

• Discharge: stable, safe, with clear instructions and follow-up
• Observation/admission: unclear diagnosis, monitoring needed, pain not controlled
• ICU: septic shock, post-ROSC, respiratory failure on ventilator, hemodynamic instability
• Transfer: if needed care (e.g., cardiothoracic surgery, neurosurgery, burn center) not available

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14. MEDICOLEGAL & PROFESSIONAL ESSENTIALS

• Document time-stamped notes for every critical decision
• Informed consent before procedures (except emergencies)
• Capacity assessment: patient can refuse care if competent
• Mandatory reporting: certain infectious diseases, gunshot wounds, child abuse
• Handover: structured SBAR (Situation, Background, Assessment, Recommendation) at shift change - verbal + written

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Treatment of COPD

Overview of Goals

• Prevent disease progression
• Relieve symptoms (dyspnea, cough, sputum)
• Improve exercise tolerance and quality of life
• Prevent and treat exacerbations
• Improve survival

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A. NON-PHARMACOLOGICAL (Foundation of All Treatment)

1. Smoking Cessation - Single Most Important Intervention

• The only proven treatment that slows the excessive decline in lung function (FEV1)
• Should be a primary and persistent goal at every patient encounter
• Approaches: behavioral counseling + pharmacotherapy (nicotine replacement, varenicline, bupropion)
• Even severely impaired patients benefit - it is never "too late"
• Physicians should address the stigma and guilt; nicotine dependence is a physical addiction, not a moral failing

2. Pulmonary Rehabilitation

• Reduces dyspnea, improves exercise capacity, reduces depression and anxiety
• Indicated for patients with MRC dyspnea grade ≥ 2 or CAT score ≥ 10
• Components: exercise training, education, nutritional support, psychological support
• ATS Clinical Practice Guideline (2023) strongly recommends pulmonary rehabilitation for adults with chronic respiratory disease (PMID 37581410)
• Also recommended immediately following a COPD exacerbation (post-exacerbation PR reduces readmission and mortality)

3. Vaccinations

• Influenza vaccine annually - reduces exacerbations and hospitalizations
• Pneumococcal vaccine (PCV13 + PPSV23) - reduces community-acquired pneumonia
• COVID-19 and Tdap vaccines as per guidelines

4. Reduce Noxious Environmental Exposures

• Occupational dust, biomass fuel smoke, air pollution
• N95 masks during high pollution days

5. Nutritional Support

• Malnutrition is common in advanced COPD and worsens prognosis
• Nutritional supplementation in underweight patients improves respiratory muscle strength

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B. PHARMACOTHERAPY - STABLE COPD (GOLD 2023 Framework)

Drug Classes

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GOLD ABE Classification & Treatment Algorithm (2023)

• SABA (salbutamol MDI 2-4 puffs PRN) for all groups as reliever/rescue
• LAMA is preferred over LABA as initial monotherapy (more effective at reducing exacerbations)
• LABA + LAMA dual therapy is superior to either alone for symptoms and exacerbations
• ICS is added (making triple therapy: ICS + LABA + LAMA) when:
  • Blood eosinophils ≥ 300 cells/µL (strong predictor of ICS benefit)
  • ≥ 2 moderate exacerbations/year OR ≥ 1 requiring hospitalization + eosinophils ≥ 100 cells/µL
  • Concurrent asthma (asthma-COPD overlap)
• Do NOT use ICS as monotherapy in COPD (increases pneumonia risk without adequate benefit alone)

Triple Therapy (ICS + LABA + LAMA)

• Single-inhaler triple therapy (e.g., fluticasone/umeclidinium/vilanterol - Trelegy Ellipta; budesonide/glycopyrrolate/formoterol - Breztri Aerosphere) significantly reduces moderate-to-severe exacerbations
• Benefits of triple therapy outweigh the small increased pneumonia risk from ICS in those with frequent exacerbations

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Roflumilast (PDE4 Inhibitor)

• Oral: 500 mcg once daily
• For GOLD 3-4 (FEV1 < 50%) with chronic bronchitis phenotype and frequent exacerbations
• Add-on to bronchodilator therapy
• Side effects: weight loss, nausea, diarrhea, depression - check for psychiatric history before starting

Azithromycin (Prophylactic)

• For patients with ≥ 3 exacerbations/year despite optimized inhaled therapy
• Azithromycin 250 mg/day or 500 mg 3x/week reduces exacerbation frequency
• Monitor: QTc prolongation, hearing loss, macrolide resistance

Theophylline

• Modest bronchodilator with anti-inflammatory properties
• Second/third line only; narrow therapeutic window (target level 8-13 mcg/mL)
• Interactions with many drugs; avoid in arrhythmias

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C. OXYGEN THERAPY

Long-Term Oxygen Therapy (LTOT)

• Indication: PaO₂ ≤ 55 mmHg OR SpO₂ ≤ 88% at rest on room air
• Or PaO₂ 56-59 mmHg with: pulmonary hypertension, cor pulmonale, hematocrit > 55%, edema from RHF
• Must be used ≥ 15 hours/day to prolong survival (based on the MRC and NOTT trials)
• Target resting SpO₂ > 90%; usual starting flow: 2 L/min via nasal cannula
• Increase flow by 1 L/min during exercise and sleep
• Air travel: if SpO₂ < 92% at rest OR < 84% on 6-min walk test → prescribe supplemental O₂ for the flight

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D. MANAGEMENT OF ACUTE EXACERBATIONS

Outpatient (Mild Exacerbation)

Antibiotic Selection for COPD Exacerbations

Criteria for Hospital Admission

• Significant increase in symptom severity
• Severe underlying COPD (FEV1 < 30%)
• Significant comorbidities (cardiac disease, pulmonary hypertension)
• Failure to respond to initial therapy
• Diagnostic uncertainty
• Insufficient home support

Criteria for ICU Admission

• Need for invasive mechanical ventilation
• Hemodynamic instability
• Severe dyspnea unresponsive to therapy
• Mental status changes (confusion, lethargy)
• Persistent or worsening hypoxemia, hypercapnia, or respiratory acidosis despite O₂ + NIV

Non-Invasive Ventilation (NIV / BiPAP) in Exacerbations

• Hypercapnic respiratory failure (PaCO₂ > 45 mmHg + respiratory acidosis pH < 7.35)
• Severe dyspnea with accessory muscle use
• RR > 25/min

Controlled Oxygen in Exacerbations

• Target SpO₂: 88-92% (NOT high-flow O₂)
• High-flow O₂ can worsen hypercapnia and cause respiratory acidosis in COPD patients (Haldane effect + Euler-Liljestrand reflex blunting)
• Use Venturi mask or titrated nasal cannula

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E. SURGICAL & INTERVENTIONAL OPTIONS

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F. SPECIAL CONSIDERATIONS

OSA-COPD Overlap Syndrome

• Patients with both OSA and COPD have higher risk of hypercapnia, pulmonary hypertension, and mortality
• Diagnose with polysomnography (PSG) with CO₂ monitoring
• Treat with CPAP or BiPAP (PAP therapy), especially if hypercapnic
• ICS may worsen OSA; theophylline may benefit

Biologics (Emerging)

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G. MONITORING & FOLLOW-UP

• Spirometry annually (or with significant symptom change) - FEV1/FVC < 0.70 post-bronchodilator confirms COPD
• 6-Minute Walk Test - functional assessment
• CAT score (COPD Assessment Test) or mMRC dyspnea scale at each visit
• Blood eosinophil count - guides ICS use
• ABG if SpO₂ < 92% on room air - assess for hypercapnia, eligibility for LTOT
• ECHO - screen for pulmonary hypertension (cor pulmonale) in advanced disease

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Summary: Stepwise Approach at a Glance

ALL PATIENTS:
Smoking cessation + Influenza/Pneumococcal vaccine + SABAs PRN

Group A (low symptoms, low risk):
+ LAMA or LABA (monotherapy)

Group B (more symptoms, low risk):
+ LABA + LAMA (dual bronchodilation)

Group E (frequent exacerbations):
+ LABA + LAMA ± ICS (if eosinophils ≥300 or ≥100 + exacerbations)
Consider: Roflumilast (chronic bronchitis, FEV1<50%), Azithromycin prophylaxis

All groups with SpO₂ ≤88%:
+ Long-term oxygen therapy ≥15 hrs/day

Advanced disease:
Pulmonary rehab + Consider LVRS / bronchoscopic valves / transplant

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Diabetic Ketoacidosis (DKA): Pathophysiology and Management

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1. DEFINITION - The Diagnostic Triad

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2. PATHOPHYSIOLOGY

INSULIN DEFICIENCY
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       ├─► Reduced glucose uptake by cells (brain uses ketones preferentially)
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       ├─► Gluconeogenesis & Glycogenolysis (liver) ──► HYPERGLYCEMIA
       |       (substrates: amino acids from muscle, lactate, pyruvate)
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       ├─► Unrestrained LIPOLYSIS (adipose tissue)
       |       ├─► Free fatty acids released into portal circulation
       |       └─► Liver converts FFAs to ketone bodies:
       |               • β-hydroxybutyrate (major - ~78%)
       |               • Acetoacetate (~20%)
       |               • Acetone (~2% - fruity breath)
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       └─► OSMOTIC DIURESIS (from hyperglycemia)
               ├─► Dehydration & hemoconcentration
               ├─► Loss of Na⁺, K⁺, Mg²⁺, PO₄³⁻, Cl⁻
               └─► Prerenal azotemia → further worsens hyperglycemia

Key Electrolyte Consequences

• Total body K⁺ is always depleted (average deficit: 3-5 mEq/kg) due to:
  • Osmotic diuresis (renal K⁺ losses)
  • Insulin deficiency (normally drives K⁺ into cells)
  • Tissue catabolism
• However, the serum K⁺ is often normal or HIGH at presentation due to acidemia shifting K⁺ out of cells
• Once insulin starts, K⁺ rapidly falls back into cells → risk of fatal hypokalemia

• Measured serum Na⁺ is factitiously LOW due to the osmotic shift of intracellular water into the extravascular space from hyperglycemia
• Correct with formula: Corrected Na⁺ = Measured Na⁺ + [1.6 × (glucose - 100)/100]
• Failure of serum Na⁺ to rise with treatment is an early warning sign of cerebral edema

• Wide anion gap metabolic acidosis: AG = Na⁺ - (Cl⁻ + HCO₃⁻); normal ≤ 12
• In DKA the AG rise should be proportional to the HCO₃⁻ fall (delta-delta ratio ~1:1)
• If HCO₃⁻ drops more than expected: coexistent non-AG acidosis (e.g., hyperchloremic or lactic acidosis)
• If HCO₃⁻ drops less than expected: coexistent metabolic alkalosis (e.g., from vomiting)

• Urine/serum dipstick (nitroprusside reaction) only detects acetoacetate, NOT β-hydroxybutyrate
• β-hydroxybutyrate is the dominant ketone in DKA, so dipstick can underestimate severity
• After insulin starts, β-OHB converts to acetoacetate → paradoxical "rise" in dipstick ketones
• Use serum β-hydroxybutyrate levels for monitoring (goal < 0.5 mmol/L)

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3. PRECIPITATING CAUSES (The "6 I's" + Drugs)

• SGLT2 inhibitor use (empagliflozin, dapagliflozin) - glucose excreted renally masking hyperglycemia
• Pregnancy, prolonged fasting, heavy alcohol use
• Pitfall: can be missed if glucose is normal

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4. CLINICAL FEATURES

• Polydipsia, polyuria (if not yet severely dehydrated)
• Nausea, vomiting, diffuse abdominal pain (can mimic acute abdomen - resolves with treatment; persistent focal tenderness suggests a surgical cause)
• Weakness, lethargy, malaise
• Blurred vision

• Kussmaul breathing - deep, sighing respirations (respiratory compensation for metabolic acidosis; can be mistaken for anxiety or pulmonary pathology)
• Fruity/acetone breath (acetone from decarboxylation of acetoacetate)
• Dehydration: dry mucous membranes, poor skin turgor, reduced JVP
• Tachycardia, orthostatic hypotension
• Depressed consciousness (ranges from alert to coma; correlates with serum osmolality)
• Hypothermia (despite infection) - sign of severe illness

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5. INVESTIGATIONS

Initial Workup

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6. MANAGEMENT - The 4 Pillars

PILLAR 1: FLUID RESUSCITATION

• Fluid deficit is typically 5-10% of body weight (3-6 litres in adults)
• Adults:
  • Start with 0.9% sodium chloride (normal saline) - even in hyperosmolar states (it is still relatively hypotonic to serum)
  • 1-2 litres in first hour for haemodynamically unstable
  • Then 1 litre/hour for 2-4 hours, then 500 mL/hour (adjust based on response)
  • Switch to 0.45% saline once Na⁺ is corrected and glucose < 250 mg/dL + add dextrose

2024 ADA Consensus Update: Balanced electrolyte solutions (e.g., Lactated Ringer's, Plasmalyte) result in faster DKA resolution and less hyperchloremic acidosis than 0.9% saline (PMID 38925619) - this is an important recent update to practice.

• Children: 20 mL/kg NS bolus over 1 hour; repeat if hypotensive; then 1.5x maintenance rate
• Add dextrose to IV fluids when glucose drops to < 250 mg/dL (without stopping insulin)

PILLAR 2: INSULIN THERAPY

• Do NOT start insulin until potassium is ≥ 3.5 mEq/L (insulin drives K⁺ into cells and can cause fatal arrhythmia if started in hypokalemia)
• No loading bolus of insulin (associated with increased cerebral edema risk)

• Fixed-rate IV insulin infusion: 0.1 units/kg/hour regular insulin
• Target glucose decline: 50-75 mg/dL/hour (do not drop faster - risk of cerebral osmotic shift)
• When glucose reaches 250 mg/dL: reduce to 0.05 units/kg/hour + add dextrose to IV fluids
• Continue insulin infusion until ketones are cleared (pH > 7.30, HCO₃ > 15, AG normalised, β-OHB < 0.5 mmol/L)

• Resolution criteria: pH > 7.30, HCO₃ > 15 mEq/L, AG normalized, patient able to eat
• Give subcutaneous long-acting insulin 1-2 hours BEFORE stopping IV insulin to prevent DKA relapse
• If patient was on background long-acting insulin, continue it throughout treatment alongside IV infusion

Recent evidence (2024-2026): Early concurrent subcutaneous basal insulin with IV infusion is associated with shorter time to DKA resolution and less rebound hyperglycemia (PMID 41208563). Subcutaneous regular insulin protocols have comparable outcomes to IV infusion in mild-moderate DKA (PMID 39090718).

PILLAR 3: ELECTROLYTE REPLACEMENT

Potassium (most critical)

• Monitor K⁺ every 2 hours during treatment
• Replace as potassium chloride (KCl) OR potassium phosphate (if phosphate also low)

Sodium

• Monitor corrected Na⁺; it should gradually rise with treatment
• Failure to rise → risk of cerebral edema (more common in children)

Phosphate

• Total body phosphate depleted but routine replacement is not proven to improve outcomes
• Replace only for symptomatic hypophosphatemia (PO₄ < 1 mmol/L with muscle weakness, respiratory depression, rhabdomyolysis)
• Give as potassium phosphate (serves dual purpose)

Bicarbonate (Sodium Bicarbonate)

• Routine use is NOT recommended - does not improve outcomes and is associated with:
  • 4x increased risk of cerebral edema
  • Paradoxical CSF acidosis (CO₂ crosses BBB faster than HCO₃⁻)
  • Accelerated hypokalemia, hypernatremia, volume overload
• Only consider if: pH < 7.0 with haemodynamic compromise unresponsive to fluids
• If given: 50 mEq NaHCO₃ over 1 hour; do not target pH > 7.1

PILLAR 4: IDENTIFY AND TREAT THE PRECIPITANT

• Cultures (blood, urine) + sepsis screen
• ECG - silent MI
• CXR - pneumonia
• Urine hCG in women of childbearing age (pregnancy + DKA is high risk)
• Review medications (SGLT2 inhibitors, steroids)

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7. MONITORING DURING TREATMENT

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8. COMPLICATIONS

Cerebral Edema (most feared, especially in children)

• Risk factors: younger age, new-onset DKA, excessive fluid administration, rapid glucose decline, failure of serum Na⁺ to rise
• Signs: headache, deteriorating consciousness, bradycardia, papilloedema, Cushing's triad
• Management: Mannitol 0.5-1 g/kg IV over 20 min OR hypertonic saline (3% NaCl 5-10 mL/kg) + reduce IV fluid rate + elevate head 30°; neurosurgical consultation

Other Complications

• Hypoglycemia - from insulin without dextrose supplementation
• Hypokalemia - fatal arrhythmias; most preventable complication
• Aspiration pneumonia - gastric dilatation + vomiting → NGT placement in obtunded patients
• Thromboembolism - DKA is prothrombotic; consider DVT prophylaxis in immobile patients
• Acute Kidney Injury - from dehydration; usually reverses with treatment
• Hyperchloremic non-AG acidosis - from large volumes of normal saline (another argument for balanced crystalloids)

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9. RESOLUTION CRITERIA

1. Blood glucose < 200 mg/dL
2. Serum HCO₃⁻ ≥ 15 mEq/L
3. Venous pH > 7.30
4. Anion gap normalized (≤ 12)
5. Serum β-hydroxybutyrate < 0.5 mmol/L (ADA 2024 updated criterion)

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10. DKA vs HHS (Quick Comparison)

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1. Check K⁺ before starting insulin - hypokalemia + insulin = cardiac arrest
2. Add dextrose to fluids at glucose 250 mg/dL, not when acidosis resolves
3. Glucose corrects faster than acidosis - keep insulin running even when glucose is normal
4. Don't use bicarbonate routinely - worsens outcomes
5. Subcutaneous overlap - give SC long-acting insulin 1-2 hours before stopping IV infusion
6. Euglycemic DKA from SGLT2 inhibitors - don't miss it because glucose is "normal"
7. Rising dipstick ketones during treatment = good sign (β-OHB → acetoacetate conversion)
8. ADA 2024 update: Use balanced crystalloids over saline and consider early concurrent SC basal insulin