MARCH Protocol Part 4: Circulation, Pelvic Fractures, and Shock Resuscitation

Following the control of catastrophic external bleeding ("M"), the securing of an uncompromised airway ("A"), and the stabilization of thoracic mechanics ("R"), Circulation ("C") shifts the tactical trauma paradigm from immediate mechanical stoppage to systemic hemodynamic resuscitation. In severe trauma, survival hinges on recognizing occult internal blood loss, stabilizing pelvic ring disruptions, restoring end-organ perfusion, and halting the lethal triad of hypothermia, acidosis, and coagulopathy.

1. Clinical Abstract & The Pathophysiology of Shock

At the physiological level, hemorrhagic shock is an acute cellular energy crisis defined by a severe deficit in systemic oxygen delivery ($DO_2$) relative to cellular oxygen consumption ($VO_2$). When circulating intravascular volume plummets from traumatic hemorrhage, capillary hydrostatic pressure collapses and cellular dysoxia begins.

Cellular Energy Depletion & Anaerobic Glycolysis

Without adequate mitochondrial oxygen delivery, cellular respiration shifts from aerobic oxidative phosphorylation (which yields 36 to 38 ATP per glucose molecule) to anaerobic glycolysis (yielding a meager 2 ATP per glucose).

• Lactic Acid Accumulation: Pyruvate is reduced to lactate, exhausting physiological serum bicarbonate buffers and creating severe metabolic lactic acidosis.
• Membrane Pump Failure: ATP depletion shuts down the energy-dependent sodium-potassium ($Na^+/K^+$ ATPase) transmembrane pump. Extracellular sodium and water rush into cells while potassium leaks into the plasma, causing cytotoxic cellular swelling, mitochondrial disruption, and cell lysis.

The Lethal Triad of Trauma

Hemorrhagic shock initiates a self-propagating vicious cycle known as the lethal triad:

2. Pelvic Ring Disruption & Circumferential Compression

Pelvic fractures caused by high-energy blunt trauma, motor vehicle crashes, structure collapses, or blast concussions represent one of the most stealthy and rapidly lethal causes of occult hemorrhagic shock.

Retroperitoneal Volume Expansion & Bleeding Dynamics

In an "open-book" pelvic ring disruption (anteroposterior compression injury), tearing of the pubic symphysis and posterior sacroiliac ligaments creates a severe mechanical expansion of the pelvis:

• Volume Doubling: The intact retroperitoneum normally accommodates approximately 4 liters of volume. With pelvic ring disruption, retroperitoneal capacity expands to over 8 liters—more than enough to exsanguinate the casualty's entire circulating blood volume internally without a single drop of visible external blood.
• Vascular Sources: 80% to 90% of pelvic hemorrhage originates from the low-pressure presacral and lumbar venous plexuses; 10% to 20% involves arterial tears to the internal iliac branches (superior gluteal, internal pudendal, obturator).

Circumferential Stabilization & The Greater Trochanter Landmark

Circumferential pelvic binders (such as the SAM Pelvic Sling II) act by anatomically reducing pelvic ring diameter, restoring retroperitoneal tamponade pressure, and immobilizing jagged bone fragments.

3. Reassessment of Massive Bleeding & Tourniquet Conversion

During the Circulation phase, the responder must systematically re-evaluate all previously placed tourniquets and hemostatic dressings:

1. Pulse Verification: Palpate the distal radial or dorsalis pedis pulse. If distal pulsation is present or bright red capillary refill continues distal to a tourniquet, the device is functioning as a venous tourniquet, accelerating blood loss. Tighten the windlass further or apply a second tourniquet immediately adjacent and proximal to the first.
2. Tourniquet Conversion Window (< 2 Hours): If evacuation to definitive surgical care is anticipated to exceed 2 hours and the casualty is hemodynamically stable without active shock, evaluate whether the extremity wound can be converted from an arterial tourniquet to a wound-packing hemostatic dressing secured by an elastic pressure wrap.
3. Strict Contraindications to Tourniquet Removal:
   • Complete or partial traumatic amputation of the limb.
   • Casualty in decompensated shock (absent radial pulse, altered mental status).
   • Tourniquet has been in place for greater than 6 hours (due to lethal reperfusion hyperkalemia and systemic myoglobin release).
   • Tactical conditions where continuous reassessment is impossible.

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4. Junctional Hemorrhage Control & Mechanical Occlusion

Junctional anatomical regions—the inguinal crease (femoral triangle), axilla (armpit), and base of the neck—cannot be effectively compressed with traditional circumferential limb tourniquets. Penetrating trauma in these zones involves high-flow vessels such as the common femoral artery and axillary artery.

• Deep Wound Packing First: The primary intervention is vigorous, continuous wound packing with a procoagulant hemostatic gauze (kaolin or chitosan-impregnated) directed straight onto the bleeding vessel against a bony backstop, maintained with at least 3 minutes of focused manual pressure.
• Targeted Pressure Pin Dynamics: Advanced dual-mode devices (such as the LST Tourniquet) utilize targeted pressure pins designed to apply localized, high-concentration mechanical force directly over the common femoral or axillary vascular bundle, occluding arterial inflow while avoiding dangerous circumferential abdominal constriction.

5. Damage Control Resuscitation & Permissive Hypotension

Damage Control Resuscitation (DCR) is a clinical strategy that prioritizes physiological survival over normal vital sign metrics during active, uncontrolled hemorrhage.

The Lethal Danger of Crystalloids

Infusing liters of normal saline (0.9% NaCl) or lactated Ringer's into a bleeding trauma casualty produces three deadly iatrogenic complications:

• Dilutional Coagulopathy: Crystalloids contain zero clotting factors, platelets, or fibrinogen, diluting natural coagulation components.
• Hyperchloremic Acidosis: Large volume normal saline induces renal vasoconstriction and exacerbates systemic metabolic acidosis.
• Mechanical Clot Disruption: Rapid spikes in hydrostatic blood pressure blow out delicate, freshly formed platelet-fibrin plugs ("popping the clot"), causing re-bleeding from previously occluded internal vessels.

Permissive Hypotension Target Blood Pressure

In casualties without traumatic brain injury (TBI), resuscitative fluid therapy is restricted to maintaining:

• Non-TBI Casualty: Titrate fluid to maintain a palpable radial pulse or a Systolic Blood Pressure (SBP) between 80 and 90 mmHg (Mean Arterial Pressure MAP ~55–65 mmHg). This pressure preserves coronary, cerebral, and renal perfusion without blowing off fragile clots.
• Traumatic Brain Injury (TBI) Exception: Injured brain tissue requires higher cerebral perfusion pressure ($CPP = MAP - ICP$). In casualties with suspected TBI, maintain an SBP ≥ 100 to 110 mmHg to prevent secondary ischemic cerebral injury.

Tranexamic Acid (TXA) Protocol

Tranexamic Acid is an antifibrinolytic lysine analogue that competitively blocks the lysine-binding sites on plasminogen, preventing its conversion to plasmin and stopping the premature enzymatic breakdown of stable fibrin clots.

• Administration Dose: 2 grams IV or IO slow push (or 1g IV bolus followed by 1g over 8 hours).
• The Strict 3-Hour Window: TXA must be administered as early as possible, and strictly within 3 hours of injury. The CRASH-2 and subsequent clinical trials established that TXA administered after 3 hours increases all-cause mortality due to late pro-thrombotic and inflammatory complications.

6. Vascular Access in the Tactical Environment: IV vs. IO

Under conditions of profound hypovolemia, peripheral veins collapse completely due to sympathetic vasoconstriction. In cold, dark, or hostile settings, standard peripheral IV cannulation fails in more than 50% of combat trauma patients, delaying life-saving blood and drug administration.

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Intraosseous (IO) Anatomy & Preferred Sites

The non-collapsible medullary venous plexus within bone functions as a rigid, non-collapsible vein that directly drains into the central venous circulation. Any medication, blood product, or fluid that can be given through an IV can be infused through an IO:

• 1. Proximal Humerus (Preferred Adult Tactical Site): Inserted into the greater tubercle of the humerus. Delivers flow rates approaching 5 L/hr under pressure and rapid delivery directly into the superior vena cava within seconds.
• 2. Proximal Tibia: Located approximately 2 cm medial and 1 cm proximal to the tibial tuberosity. Highly visible bony landmark, but produces lower flow rates (~1 L/hr) due to peripheral limb resistance.
• 3. Sternal Site: Used with specialized sternal devices (e.g., FAST1), offering reliable flow but precluding chest compressions and interfering with anterior chest trauma management.

7. MED-TAC 3-Tier Product Ladder Integration

Circulation and shock management hardware is structured across three tiers of operational capability:

8. Clinical Frequently Asked Questions