Critical Care Medicine – Study Notes (Part 1)
Oxygen Content & Delivery
Physiologic Goal
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Oxygen’s end-point: mitochondrial ATP production.
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Hypoxemia/desaturation → ↓ ATP, failure of membrane integrity → apoptosis/necrosis.
Oxygen Gradient
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Required across all steps: atmosphere → alveoli → arterial blood → tissues → mitochondria.
Oxygen Transport
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Carried mostly by hemoglobin, with a small dissolved fraction.
O₂ Content Formula:
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Hemoglobin & saturation = main determinants.
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PaO₂ contributes little.
Hemoglobin–Oxygen Binding
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Influenced by p50 (~26 mmHg).
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Right shift (↑ p50, ↓ affinity): acidosis, ↑ temperature, ↑ CO₂, ↑ 2,3-DPG.
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Left shift (↓ p50, ↑ affinity): alkalosis, ↓ temperature, ↓ CO₂, ↓ 2,3-DPG.
Oxygen Delivery (DO₂)
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Cardiac output × oxygen content (×10 for unit correction).
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DO₂ is what matters clinically.
Oxygen Consumption (VO₂)
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Normal ≈ 250 mL/min (varies).
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Measured by direct or indirect calorimetry (metabolic cart).
Fick Principle:
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Must use oxygen content, not just saturation.
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Errors: using venous saturation instead of content.
VO₂ increased by: sepsis, hyperthyroidism, seizures, shivering, fever, malignant hyperthermia.
VO₂ decreased by: anesthesia, neuromuscular blockade, hypothyroidism, hypothermia.
Mechanical Ventilation
Non-Invasive Ventilation
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BiPAP: improves both ventilation (↑ IPAP) and oxygenation (↑ EPAP).
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CPAP: improves oxygenation only; classically for cardiogenic pulmonary edema.
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Contraindications: altered mental status, vomiting/aspiration risk, bowel obstruction, gastroparesis.
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High-flow nasal cannula (HFNC) increasingly replacing CPAP.
Ventilatory Cycle
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Trigger → Inspiratory flow → Cycle → Expiration.
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Triggers: machine, pressure, flow.
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Cycling: volume, time, flow, or pressure.
Ventilation Modes
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Volume Control: constant tidal volume; variable pressures.
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Pressure Control: constant pressure; variable tidal volume.
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Assist Control (AC): minimum set rate + patient-triggered breaths.
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SIMV: mandatory breaths + spontaneous breaths (may add pressure support).
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Pressure Support: fully patient-driven; no backup rate (except apnea safety mode).
Key Pressures
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Peak Inspiratory Pressure (PIP): resistance + compliance.
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Plateau Pressure: compliance only (measured during inspiratory pause).
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Interpretation:
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High PIP, normal plateau → resistance problem.
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High PIP & plateau → compliance problem.
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PEEP (Positive End-Expiratory Pressure)
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Prevents alveolar derecruitment.
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Improves oxygenation but ↑ intrathoracic pressure → ↓ venous return.
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Overdistension risk if too high.
ARDS (Acute Respiratory Distress Syndrome)
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Non-cardiogenic pulmonary edema due to inflammatory injury of alveolo-capillary membrane.
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Heterogeneous distribution in lungs.
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Causes: pneumonia, aspiration, trauma, burns, pancreatitis, sepsis.
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CXR: bilateral infiltrates, diffuse.
No curative treatment.
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Focus = treat underlying cause + supportive care.
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Lung-protective ventilation:
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Low tidal volume (6 mL/kg IBW).
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Plateau pressure < 30 cmH₂O.
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Avoid volutrauma/barotrauma.
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Inhaled nitric oxide: may transiently improve oxygenation, but no mortality benefit. Rescue use only.
Infection Control in Critical Care
Precautions
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Standard: baseline for all patients.
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Contact: gown/gloves.
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Droplet: surgical mask.
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Airborne: N95, negative pressure.
Ventilator-Associated Pneumonia (VAP)
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From microaspiration around ETT cuff.
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Organisms differ from community pneumonia.
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Specialized ETTs may help but limited mortality impact.
VAP Prevention Bundle:
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Daily sedation breaks / awakening trials.
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Early extubation.
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Stress ulcer prophylaxis.
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DVT prophylaxis.
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Chlorhexidine oral care.
Central Line–Associated Bloodstream Infection (CLABSI)
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Caused by poor insertion or maintenance.
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Prevention Bundle:
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Hand hygiene.
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Full barrier precautions (cap, gown, mask, sterile gloves, full drape).
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Chlorhexidine skin prep.
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Daily assessment & prompt removal when no longer needed.
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Antimicrobial discs/occlusive dressings reduce risk.
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Anesthesia Keyword Review – Critical Care (Part 2 of 2)
Topics Covered
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Shock states
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Sepsis
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Resuscitation & fluids
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Nutrition
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Burns
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Drowning
Shock States
Definition
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Circulatory shock = syndrome of reduced tissue perfusion.
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Not just hypotension → key problem = inadequate capillary blood flow to supply O₂ + glucose for ATP production.
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Result: electrolyte imbalance → cell membrane pump failure → ischemia → infarction → necrosis.
Mortality
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Still very high.
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Septic or cardiogenic shock: mortality may reach ~50%.
Phases of Shock
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Reversible/Early Shock
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Reflexes (macro/microvascular + cellular + immunologic) try to preserve cardiac output & arterial pressure.
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Organ dysfunction absent or minimal.
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Late Shock
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Perfusion of heart/major organs begins to fail.
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Organ dysfunction becomes obvious.
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Not a sharp cutoff; continuum.
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Irreversible/Terminal Shock
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Vasomotor dysfunction, loss of arteriolar tone.
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Paradoxical ↑ central venous tone (pathologic).
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Ischemia → infarct → necrosis.
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Types of Shock
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Distributive (hyperdynamic)
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↑ Cardiac output.
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↓ SVR.
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↑ Mixed venous saturation.
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↓ Wedge pressure.
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Ex: Septic shock.
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Hypovolemic
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↓ CO, ↑ SVR.
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↓ Mixed venous saturation.
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↓ Wedge pressure.
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Cardiogenic
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↓ CO, ↑ SVR.
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↓ Mixed venous saturation.
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↑ Wedge pressure.
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Obstructive
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↓ CO, ↑ SVR.
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↓ Mixed venous saturation.
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↑ Wedge pressure.
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Sepsis & Septic Shock
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Distributive shock subtype.
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Pathophysiology: dysregulated host immune response, pro-inflammatory imbalance.
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Genetics: influence severity/outcome.
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Early recognition = survival.
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Treat septic shock like a code (time-critical).
Definitions
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Sepsis definitions evolving (Sepsis-3 replaced SIRS-based).
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Still: infection → systemic inflammation → sepsis → septic shock (hypotension + tissue malperfusion).
Management Principles
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Initial resuscitation: aggressive fluids + vasopressors if needed.
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Antibiotics: broad spectrum within 1 hour of symptom onset.
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Blood cultures first if possible (then urine → lung).
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De-escalate once pathogen identified.
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Source control: drain abscess, remove infected hardware.
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Fluids:
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Crystalloids preferred (no consistent advantage to colloids).
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May require 10–14 L/24 hrs early.
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Remove excess fluid aggressively by day 2–3.
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Hemodynamic goals: MAP ≥ 65 mmHg.
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Vasopressors:
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1st line = norepinephrine.
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Add vasopressin to reduce norepi dose.
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Rescue = epinephrine.
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Inotropes:
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Dobutamine if myocardial dysfunction + low CO.
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Avoid supraphysiologic oxygen delivery goals.
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Steroids:
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Consider if refractory to catecholamines.
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Watch for hyperglycemia.
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Resuscitation Fluids
Crystalloids vs Colloids
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No mortality difference overall.
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Colloids (albumin) indicated in specific conditions:
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Cirrhosis + SBP (spontaneous bacterial peritonitis).
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Hepatorenal syndrome.
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Large-volume paracentesis.
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Hydroxyethyl starches (HES): avoided (coagulopathy, AKI risk).
Crystalloids
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Options: D5W, ½NS, NS, LR, Plasma-Lyte.
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Electrolyte content varies.
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Balanced solutions (LR, Plasma-Lyte) preferred for large resuscitation.
Nutrition in Critical Care
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Enteral (preferred) over TPN when possible.
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Improves mortality, ↓ infection, ↓ ventilator days.
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TPN (yellow bag): hypertonic glucose, amino acids, electrolytes, vitamins, lipids.
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Indications: short gut, high-output fistula, prolonged obstruction or ileus.
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Complications: infection (CLABSI), liver dysfunction, cholelithiasis, refeeding syndrome, hyperglycemia.
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Caloric needs: ~25 kcal/kg/day (↑ in burns, trauma, sepsis).
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Protein needs: 1.5–2 g/kg/day (↑ in burns, trauma, AKI).
Burns
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Cause massive inflammation and fluid loss.
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Airway management:
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Intubate early if facial soot, singed nasal hairs, mouth burns → prevent airway edema obstruction.
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Fluid resuscitation: Parkland formula (starting point, not absolute).
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Neuromuscular blockade considerations:
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Succinylcholine contraindicated after 24–48 hrs (risk hyperkalemia).
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Resistance to non-depolarizers possible.
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Drowning
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Primary cause of death: hypoxemia from aspiration.
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Even if rescued: risk of ARDS, inflammation.
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Hypothermia common (even in non-arctic water).
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Cardiogenic shock possible (↑ CVP/wedge with immersion).
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Always evaluate for secondary injuries (trauma → spinal cord injury, internal lacerations).
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