Damage Control Resuscitation

DCR Fundamentals - Shock & Awe Management

• Goal: Rapid hemorrhage & contamination control; restore physiology. Prevent/reverse "Lethal Triad."
• Indications: Severe trauma (e.g., penetrating torso), MTP activation, profound shock.
  • Physiologic Triggers: Temp < 35°C; pH < 7.2; Base Deficit > 6 mEq/L; INR > 1.5.
• Lethal Triad: Vicious cycle of:
  • Hypothermia (< 35°C)
  • Acidosis (pH < 7.2)
  • Coagulopathy (INR > 1.5; PTT > 60s) 📌 Mnemonic: Acidosis, Bleeding (Coagulopathy), Cold (Hypothermia).

⭐ The Lethal Triad (hypothermia, acidosis, coagulopathy) is a primary target of DCR; breaking this cycle early is critical for survival.

Permissive Hypotension - Low Flow, High Stakes

• Aim: Limit hemorrhage, prevent clot disruption, avoid dilutional coagulopathy pre-operatively.
• Targets:
  • SBP: 80-100 mmHg
  • MAP: 50-70 mmHg
• Rationale: ↓ hydrostatic pressure at injury site → ↓ bleeding.
• Key Exclusions:
  • ⚠️ Traumatic Brain Injury (TBI)
  • Spinal cord injury
  • Caution: Elderly, chronic hypertension.
• Endpoint: Until surgical hemostasis achieved; then normalize BP.

⭐ Contraindicated in TBI to maintain Cerebral Perfusion Pressure (CPP); target higher MAP in TBI to prevent secondary brain injury.

Hemostatic Resuscitation - Balancing Act

Core aim: Restore circulating volume & correct coagulopathy with blood products in whole blood ratios, minimizing crystalloids.

• Key Components & Targets:
  • Ratio-driven: Target 1:1:1 PRBCs:FFP:Platelets.
  • Tranexamic Acid (TXA): Early 1g IV (10 min), then 1g IV (8 hrs).
  • Calcium: Monitor & replete ionized Ca (target >1.1 mmol/L) for citrate toxicity.
  • Goal-Directed: Use Viscoelastic Hemostatic Assays (VHA) like TEG/ROTEM if available.
  • Restrict Crystalloids: Avoid dilutional coagulopathy, acidosis.

⭐ CRASH-2 Trial: TXA within 3 hours of injury significantly reduces mortality and death due to bleeding in trauma patients.

Anesthesia in DCR - Controlled Chaos

• Goals: Rapid control, facilitate surgery, support resuscitation.
• Induction:
  • Ketamine (1-2 mg/kg IV): Preferred for hemodynamic stability.
  • Etomidate (0.2-0.3 mg/kg IV): Cardiac stable; caution: adrenal suppression.
  • Minimize propofol/thiopentone (risk of hypotension).
• Maintenance:
  • Volatiles at low MAC (<0.5) or TIVA (e.g., ketamine infusion).
  • Adequate analgesia (opioids).
• Relaxants:
  • RSI common: Succinylcholine (1-1.5 mg/kg) or Rocuronium (0.9-1.2 mg/kg).
• Monitoring: Standard ASA, invasive BP, CVP, temp, UO. Consider TEG/ROTEM.
• Ventilation: Lung protective ($V_T$ 6-8 mL/kg IBW), permissive hypercapnia (if no TBI).
• Challenges: Lethal triad (hypothermia, acidosis, coagulopathy), aspiration risk.

⭐ Ketamine is favored for induction in DCR due to its sympathomimetic properties, aiding hemodynamic stability in critically injured patients.

DCS & ICU Phase - The Bigger Picture

• DCR enables Damage Control Surgery (DCS): rapid, abbreviated surgery for hemorrhage/contamination control, deferring definitive repair.
• DCS aims for physiological stabilization before complete anatomical correction.
• ICU: Ongoing resuscitation, correct Lethal Triad (acidosis, hypothermia, coagulopathy), optimize for staged procedures.
• Essential: multidisciplinary team for OR-ICU-definitive care continuum.

⭐ Key DCS strategy: Temporary Abdominal Closure (TAC) for planned re-exploration & managing compartment syndrome.

High‑Yield Points - ⚡ Biggest Takeaways

• DCR combats the "triad of death": hypothermia, acidosis, and coagulopathy.
• Employs permissive hypotension (target SBP 80-90 mmHg) until bleeding controlled, contraindicated in TBI.
• Prioritizes balanced resuscitation with 1:1:1 ratio of PRBCs:FFP:Platelets via MTP.
• Minimizes crystalloid infusion to prevent dilutional coagulopathy & ACS.
• Administer tranexamic acid (TXA) early (within 3 hours) to reduce bleeding.
• Integral to Damage Control Surgery (DCS) for rapid physiological stabilization.