Hemorrhage Control and Traumatic Shock - NREMT Paramedic Level

SECTION 1

Historical Context & Motivation

Uncontrolled hemorrhage has been the leading preventable cause of death on battlefields and in civilian trauma for centuries. Early military surgeons recognized that soldiers who bled profusely after limb injuries could sometimes survive if pressure or a ligature was applied rapidly, yet the underlying physiology of traumatic shock remained poorly understood until the twentieth century. The evolution from crude tourniquets wrapped around musket-shattered limbs to evidence-based, protocolized hemorrhage control represents one of the most impactful advances in emergency medicine. Each major armed conflict produced innovations that subsequently reshaped civilian prehospital care, and modern paramedic practice stands on those hard-won lessons.

1674 • Morel's Field Tourniquet

French military surgeon Étienne Morel developed a practical windlass tourniquet for battlefield extremity hemorrhage, establishing the principle of mechanical vascular occlusion that persists in modern devices such as the CAT (Combat Application Tourniquet).

1899 • Crile Describes Surgical Shock

George W. Crile published foundational research differentiating hemorrhagic shock from neurogenic shock, establishing that volume depletion—not 'nervous exhaustion'—drives cardiovascular collapse after trauma.

1941–1945 • WWII Blood Banking & Resuscitation

Mass adoption of stored whole blood, plasma, and crystalloid resuscitation in forward surgical hospitals dramatically lowered mortality rates and laid the groundwork for modern fluid resuscitation protocols.

2005 • TCCC Tourniquet Mandate

The Committee on Tactical Combat Casualty Care (TCCC) formally endorsed early tourniquet use for all compressible extremity hemorrhage, reversing decades of civilian EMS reluctance and reducing preventable battlefield deaths by an estimated 70%.

2015–Present • Stop the Bleed & Whole-Blood Prehospital Programs

The American College of Surgeons launched the Stop the Bleed campaign, while prehospital whole-blood transfusion programs expanded across civilian EMS, aligning field care with damage-control resuscitation principles.

The central question that drives this lesson is deceptively straightforward: how does a paramedic identify that a patient is bleeding to death—often when external blood loss is minimal—and what interventions, performed in the correct sequence, can arrest that lethal cascade before the patient reaches definitive surgical care?

SECTION 2

Core Principles & Definitions

Understanding hemorrhage control and traumatic shock requires mastery of several interlocking physiological and clinical concepts. The human cardiovascular system can tolerate small volume losses through compensatory mechanisms—tachycardia, peripheral vasoconstriction, and increased myocardial contractility—but when these reserves are exhausted, the patient enters decompensated shock, a rapidly fatal trajectory. The paramedic's role is to intervene during the compensatory phase, or as early as possible in decompensation, using a combination of mechanical hemorrhage control and targeted resuscitation.

Hemorrhagic Shock Classification

The American College of Surgeons classifies hemorrhagic shock into four classes (I–IV) based on estimated blood loss, heart rate, blood pressure, respiratory rate, mental status, and urine output. Each class corresponds to escalating interventions.

Compressible vs. Non-Compressible Hemorrhage

Compressible hemorrhage arises from extremity, scalp, or external junctional wounds amenable to direct pressure, tourniquets, or hemostatic dressings. Non-compressible hemorrhage originates from thoracic, abdominal, or pelvic cavities and requires surgical or interventional radiology control.

Lethal Triad of Trauma

The lethal triad consists of hypothermia, acidosis, and coagulopathy. Each element potentiates the others in a positive-feedback loop that accelerates hemorrhage and organ failure unless actively interrupted.

Damage-Control Resuscitation

Damage-control resuscitation (DCR) emphasizes permissive hypotension, limited crystalloid use, early blood product administration (ideally in a 1:1:1 ratio of packed RBCs, plasma, and platelets), and aggressive prevention of hypothermia.

Shock Index

The Shock Index (SI) is calculated as heart rate divided by systolic blood pressure. A normal SI is approximately 0.5–0.7; values exceeding 1.0 strongly suggest significant hemorrhage even when vital signs appear individually acceptable.

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KEY TAKEAWAY

Think of the cardiovascular system like a closed hydraulic circuit in an industrial machine. The heart is the pump, the vasculature is the piping, and the blood is the hydraulic fluid. A small leak (Class I hemorrhage) can be compensated by increasing pump speed and narrowing pipes, but once fluid drops below a critical level, the entire system loses pressure catastrophically—that is decompensated shock. Your job as a paramedic is to seal the leak and maintain just enough fluid to keep the circuit functional until a mechanic (surgeon) can perform a definitive repair.

SECTION 3

Visual Explanation — Hemorrhagic Shock Pathophysiology

This diagram illustrates the four classes of hemorrhagic shock progressing from left (compensated, Class I) to right (irreversible, Class IV). Below, the four major categories of prehospital hemorrhage interventions are shown alongside the lethal triad of hypothermia, acidosis, and coagulopathy that must be aggressively countered during resuscitation.

As the diagram makes clear, the transition from Class II to Class III is the critical inflection point: systolic blood pressure finally drops, mental status deteriorates, and the compensatory mechanisms that masked hemorrhage begin to fail. Notice that Class I and Class II shock share similar blood pressure readings—this is why relying on systolic BP alone is dangerously misleading. The Shock Index (heart rate ÷ systolic BP) and serial assessments of mental status and capillary refill are far more sensitive early indicators. The intervention boxes highlight that hemorrhage control always takes priority: no amount of IV fluid will save a patient whose bleeding source is not addressed.

SECTION 4

Physiological Mechanisms & Key Calculations

The hemodynamic consequences of hemorrhage can be quantified through several interconnected equations that every paramedic should understand, not merely memorize. These relationships explain why certain clinical findings emerge at specific volume-loss thresholds and why targeted interventions work.

CARDIAC OUTPUT

CO = SV × HR

Where CO = cardiac output (L/min), SV = stroke volume (mL/beat), and HR = heart rate (beats/min). In early hemorrhage, SV drops as preload decreases, so the sympathetic nervous system increases HR to maintain CO. When HR can no longer compensate, CO falls and hypotension ensues.

MEAN ARTERIAL PRESSURE

MAP = CO × SVR

Where MAP = mean arterial pressure (mmHg) and SVR = systemic vascular resistance. Sympathetic-mediated vasoconstriction initially increases SVR to preserve MAP despite falling CO. A MAP below 65 mmHg is generally insufficient for end-organ perfusion.

SHOCK INDEX

SI = HR / SBP

Where SI = Shock Index, HR = heart rate, and SBP = systolic blood pressure. An SI > 0.9 in trauma patients correlates with the need for massive transfusion, and an SI > 1.0 strongly predicts mortality if hemorrhage is not controlled.

ESTIMATED BLOOD LOSS (EBL)

EBL = EBV × (Hct₁ − Hct₂) / Hct₁

Where EBV = estimated blood volume (≈ 70 mL/kg in adults), Hct₁ = baseline hematocrit, and Hct₂ = current hematocrit. This formula is most useful in the hospital setting; in the field, the shock class and clinical presentation guide volume-loss estimation.

These equations reveal the interconnected nature of shock physiology. As hemorrhage reduces circulating volume, preload drops (Frank-Starling mechanism), which lowers stroke volume. Baroreceptors in the carotid sinus and aortic arch trigger a sympathetic response that increases heart rate and systemic vascular resistance. If the hemorrhage source is not controlled, these compensatory mechanisms are eventually overwhelmed—cardiac output plummets, MAP falls below perfusion thresholds, and the cascade of anaerobic metabolism, lactic acidosis, and coagulopathy begins.

SECTION 5

Hemorrhage Classification & Management Algorithm

Parameter	Class I	Class II	Class III	Class IV
Blood Loss (mL)	< 750	750–1,500	1,500–2,000	> 2,000
% Blood Volume	< 15%	15–30%	30–40%	> 40%
Heart Rate	< 100	100–120	120–140	> 140
Systolic BP	Normal	Normal	Decreased	Very Low
Respiratory Rate	14–20	20–30	30–40	> 35
Mental Status	Slightly anxious	Mildly anxious	Anxious/confused	Lethargic
Urine Output	> 30 mL/hr	20–30 mL/hr	5–15 mL/hr	Negligible
Fluid Replacement	Crystalloid	Crystalloid	Crystalloid + Blood	Massive Transfusion

ATLS Hemorrhagic Shock Classification (adapted from ACS)

This decision-tree algorithm guides prehospital providers through hemorrhage control in a stepwise fashion: identify the hemorrhage, determine whether it is life-threatening and compressible, select the appropriate intervention (direct pressure, tourniquet, wound packing with hemostatics, or junctional device), reassess, and escalate as necessary before initiating resuscitation and rapid transport.

The algorithm underscores a critical hierarchy: hemorrhage control always precedes fluid resuscitation. There is no benefit to pouring fluid into a system that is still leaking. For extremity hemorrhage, a tourniquet applied 2–3 inches proximal to the wound (or 'high and tight' in tactical settings) is first-line therapy. For junctional hemorrhage at the axilla, groin, or neck, wound packing with a hemostatic agent such as kaolin-impregnated gauze (QuikClot Combat Gauze) is preferred, supplemented by junctional tourniquet devices when available. Truncal hemorrhage—thoracic, abdominal, or retroperitoneal—is non-compressible from the outside and requires rapid transport to surgical intervention. Tranexamic acid (TXA) should be administered intravenously within three hours of injury (ideally within one hour) at a dose of 1 g IV over 10 minutes to inhibit fibrinolysis and support clot stability.

SECTION 6

Worked Example — Prehospital Trauma Scenario

SCENARIO: MOTORCYCLE COLLISION WITH BILATERAL LOWER EXTREMITY TRAUMA

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Step 1 — Scene Assessment & Initial Findings

You arrive at a motorcycle collision. The patient is a 32-year-old male, approximately 80 kg, found supine on the roadway with an open femur fracture on the right leg and significant arterial bleeding from a deep laceration to the left thigh. The scene is safe. Your partner applies manual c-spine stabilization while you perform a rapid primary assessment. The patient is conscious but confused, diaphoretic, and pale. Initial vitals: HR 132, BP 82/54, RR 34, SpO₂ 94% on room air.

Shock Index = 132 ÷ 82 = 1.61 → consistent with Class III–IV hemorrhagic shock
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Step 2 — Immediate Hemorrhage Control

Both wounds are on the extremities and are compressible. Apply a CAT tourniquet to the left thigh, 2–3 inches proximal to the laceration. Tighten the windlass until arterial bleeding stops. Note the time: 14:32. For the open femur fracture on the right leg with associated hemorrhage, apply a second tourniquet to the right thigh proximal to the fracture site. If available, pack the open wound with hemostatic gauze before applying the tourniquet. Document both tourniquet times.

Two tourniquets applied: Left thigh 14:32, Right thigh 14:33. Bleeding controlled bilaterally.
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Step 3 — Estimate Blood Volume & Loss

Estimated blood volume (EBV) for an 80 kg adult male = 80 × 70 mL/kg = 5,600 mL. Given the clinical presentation (tachycardia > 120, hypotension, confusion, tachypnea > 30), the patient is in Class III to early Class IV hemorrhagic shock, corresponding to approximately 1,500–2,500 mL of blood loss (27–45% of circulating volume). The altered mental status and significant tachycardia strongly suggest losses exceeding 30%.

Estimated blood loss: approximately 1,700–2,200 mL (≈ 30–40% of EBV)
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Step 4 — Resuscitation & Adjuncts

Establish two large-bore (14–16 gauge) IV lines. If your service carries prehospital blood products, initiate transfusion per protocol. Otherwise, administer a 500 mL crystalloid bolus and reassess—target a systolic BP of 80–90 mmHg (permissive hypotension) rather than normotension, to avoid disrupting fragile clots. Administer tranexamic acid (TXA) 1 g IV over 10 minutes. Apply a pelvic binder as a precaution given the mechanism. Actively prevent hypothermia: remove wet clothing, apply a hypothermia blanket, and warm IV fluids if available.

TXA administered at 14:36. Permissive hypotension target: SBP 80–90 mmHg. Active warming initiated.
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Step 5 — Reassessment & Transport Decision

Reassess after hemorrhage control and initial fluid bolus. Repeat vitals at 14:40: HR 118, BP 86/58, RR 28, SpO₂ 96% on supplemental O₂. The shock index has improved from 1.61 to 1.37—still significantly elevated, confirming ongoing need for definitive care. The patient remains confused but is responding to questions. Transport emergently to a Level I trauma center. Call ahead for massive transfusion protocol activation. Continuously reassess tourniquet effectiveness and vital signs en route, providing additional crystalloid or blood products as indicated by your protocol.

Transport initiated 14:42. Trauma center notified, MTP activated. SI improving but still critical at 1.37.

SECTION 7

Hemorrhage Control Methods — Strengths & Limitations

Intervention	Strengths	Limitations
Direct Pressure	Universal first-line; no equipment needed; effective for most minor to moderate wounds; low risk of complications.	Requires sustained manual effort; ineffective for arterial extremity hemorrhage; ties up a provider's hands; not practical for junctional or deep wounds.
Tourniquet (CAT, SOFTT-W)	Rapid application (< 30 sec); highly effective for extremity arterial hemorrhage; frees provider hands; evidence-based survival benefit.	Only effective on extremities; can cause nerve damage or ischemia if left > 6 hours; painful for the patient; not indicated for junctional or truncal bleeding.
Hemostatic Agents (QuikClot, Celox)	Effective in junctional and deep wounds; promotes clot formation; can be used with wound packing in areas not amenable to tourniquet.	Requires wound packing technique training; some older formulations were exothermic (risk of thermal injury); must be held with pressure for 3–5 min; limited utility in body cavities.
Junctional Devices (JETT, SAM Junctional)	Addresses the axilla/groin 'tourniquet gap'; can apply targeted pressure to inguinal or axillary vessels; useful for pelvic hemorrhage.	Bulky; requires training; not universally carried on ambulances; limited evidence base compared to tourniquets; not effective for intra-abdominal bleeding.
Pelvic Binder	Stabilizes pelvic ring fractures; reduces pelvic volume to tamponade venous hemorrhage; quick to apply; low complication rate.	Does not control arterial pelvic hemorrhage; contraindicated in open-book fractures with pubic symphysis overlap; does not replace surgical fixation.
TXA (Tranexamic Acid)	Reduces fibrinolysis; decreases mortality when given within 3 hours (CRASH-2 trial); easy IV administration; synergistic with mechanical control.	Must be given early (benefit declines after 3 hours, potentially harmful after); does not control hemorrhage mechanically; not a substitute for surgical hemostasis.

Comparison of Prehospital Hemorrhage Control Interventions

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KEY TAKEAWAY

No single hemorrhage control tool works in every anatomical context. Think of your interventions like a toolbox: a tourniquet is the wrench that perfectly fits extremity bolts, hemostatic gauze is the sealant for irregular junctional gaps, and TXA is the thread-locker that keeps everything from coming undone at the molecular level. The paramedic who reaches for the right tool at the right time—without hesitation—is the one who saves lives in the platinum ten minutes of prehospital trauma care.

SECTION 8

Connecting Prehospital Care to Damage-Control Surgery

Prehospital hemorrhage control and resuscitation are the first links in a continuum known as damage-control surgery (DCS). While the paramedic addresses compressible hemorrhage and initiates permissive hypotension, the trauma surgeon performs an abbreviated laparotomy or thoracotomy focused solely on hemorrhage control and contamination containment, deferring definitive repair to later operations when the patient is physiologically optimized. Understanding this philosophy helps the paramedic appreciate why excessive crystalloid administration in the field is detrimental—it dilutes clotting factors, lowers core temperature, and raises blood pressure enough to disrupt nascent clots, all of which complicate the surgeon's task.

Concept	Prehospital (Paramedic)	In-Hospital (Trauma Surgery)
Hemorrhage Control	Tourniquets, wound packing, hemostatic agents, junctional devices, pelvic binders	Surgical ligation, embolization, damage-control laparotomy/thoracotomy, REBOA
Resuscitation Strategy	Permissive hypotension (SBP 80–90), limited crystalloid, prehospital blood if available, TXA	Massive transfusion protocol (1:1:1 RBC:FFP:Plt), calcium supplementation, targeted TEG/ROTEM-guided therapy
Hypothermia Prevention	Remove wet clothing, warming blankets, warm IV fluids	Warmed operating room, rapid infuser with inline warming, warmed irrigation fluids
Acidosis Management	Restore perfusion via hemorrhage control; ventilation support	Sodium bicarbonate if pH < 7.1; restore CO via surgical hemostasis; ICU resuscitation endpoints (lactate clearance)
Monitoring	Shock Index, mental status, capillary refill, EtCO₂, serial vitals	Arterial line, CVP, serial lactate, base deficit, TEG/ROTEM, urine output

Prehospital vs. In-Hospital Hemorrhage & Shock Management

Emerging technologies such as Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) and lyophilized plasma are beginning to bridge the gap between prehospital and surgical hemorrhage control. Some advanced EMS systems are trialing prehospital REBOA for non-compressible truncal hemorrhage, and freeze-dried plasma products promise to bring the benefits of balanced resuscitation to the field without the cold-chain logistics of liquid blood products. As a future paramedic, your understanding of damage-control resuscitation principles positions you to adopt these evolving therapies as they enter clinical practice.

SECTION 9

Practice Problems

Question 1: CONCEPTUAL

Explain why a patient in Class II hemorrhagic shock may present with a normal systolic blood pressure despite having lost up to 30% of their circulating blood volume. What compensatory mechanisms are at work, and how would you identify this 'occult' shock in the field?

Show answer

In Class II hemorrhagic shock, the body activates powerful sympathetic compensatory mechanisms: baroreceptor-mediated release of catecholamines increases heart rate (tachycardia to 100–120 bpm) and systemic vascular resistance through peripheral vasoconstriction. These responses maintain cardiac output and mean arterial pressure at near-normal levels despite a 15–30% volume deficit. In the field, you should look beyond systolic BP and calculate the Shock Index (HR ÷ SBP); a value > 0.9 suggests significant hemorrhage. Additionally, serial assessments of mental status (mild anxiety), capillary refill (> 2 seconds), skin color (pale, diaphoretic), narrowed pulse pressure, and respiratory rate (> 20) are more sensitive early indicators than systolic BP alone.

Question 2: BASIC CALCULATION

A 70 kg adult female presents after a stabbing injury with a heart rate of 128 and a systolic blood pressure of 78 mmHg. Calculate her Shock Index, estimate her blood volume, and determine the approximate class of hemorrhagic shock based on her presentation.

Show answer

Shock Index = HR ÷ SBP = 128 ÷ 78 = 1.64. This is significantly elevated (normal is 0.5–0.7), indicating severe hemorrhage. Her estimated blood volume is 70 kg × 70 mL/kg = 4,900 mL. With a heart rate of 128 (> 120), a systolic BP of 78 (decreased), and an SI of 1.64, she is in Class III hemorrhagic shock, corresponding to approximately 30–40% blood volume loss, or roughly 1,470–1,960 mL. The hypotension confirms she has exceeded the compensatory phase. Immediate hemorrhage control and fluid resuscitation with blood products are indicated.

Question 3: INTERMEDIATE

You are treating a patient with a gunshot wound to the left groin area with arterial hemorrhage. A standard extremity tourniquet cannot be placed proximal to the wound due to the inguinal location. Describe, in order, the hemorrhage control interventions you would attempt and the rationale for each.

Show answer

Junctional hemorrhage at the inguinal crease is a classic 'tourniquet gap' injury. First, apply direct manual pressure to the wound site while you prepare your next intervention. Second, pack the wound tightly with hemostatic gauze (e.g., QuikClot Combat Gauze), pushing the gauze directly into the wound cavity against the bleeding vessel, and hold firm pressure for a minimum of 3 minutes. Third, if a junctional tourniquet device is available (e.g., SAM Junctional Tourniquet or JETT), apply it over the inguinal region to provide sustained mechanical compression of the common femoral artery. Fourth, administer TXA 1 g IV over 10 minutes if within 3 hours of injury. Throughout, reassess for continued bleeding. If hemorrhage persists despite these measures, maintain maximal packing and pressure during emergent transport to a trauma center for surgical control. The rationale is that junctional wounds require a layered approach because no single mechanical device reliably occludes vessels at the junction of the torso and extremity.

Question 4: APPLIED

During a prolonged extrication from a vehicle accident, you have a patient with bilateral femur fractures and controlled external hemorrhage, but he is becoming progressively more confused and tachycardic despite two tourniquets and 500 mL of crystalloid. His skin is cold, core temperature reads 34.8°C, and his SpO₂ is 92%. Describe how the lethal triad is developing and outline your comprehensive management strategy.

Show answer

This patient is developing the lethal triad of trauma. First, hypothermia (34.8°C) is caused by exposure, hemorrhage-related hypoperfusion, and ambient cooling during extrication. Hypothermia impairs the coagulation cascade by slowing enzymatic reactions, worsening bleeding. Second, hemorrhage and hypoperfusion shift metabolism to anaerobic pathways, producing lactic acid and metabolic acidosis. Acidosis further impairs clotting factor function and myocardial contractility. Third, the combination of hypothermia and acidosis, plus dilution from crystalloid and consumption of clotting factors at injury sites, produces coagulopathy—worsening hemorrhage and completing the positive-feedback loop. Your management strategy should include: (1) Reassess tourniquet effectiveness—ensure they are still achieving arterial occlusion; (2) Stop all crystalloid and switch to blood products if available, as crystalloid dilutes clotting factors and lacks oxygen-carrying capacity; (3) Aggressively rewarm: remove wet clothing, apply a hypothermia prevention kit or warm blankets, warm IV fluids through an inline warmer; (4) Administer TXA if not already given; (5) Optimize ventilation with supplemental oxygen and consider assisted ventilation to address hypoxia; (6) Minimize scene time—coordinate with rescue teams to expedite extrication and transport to a Level I trauma center with MTP pre-activation. Breaking even one arm of the lethal triad can interrupt the cascade.

Question 5: CRITICAL THINKING

The CRASH-2 trial demonstrated that TXA reduces mortality in hemorrhaging trauma patients when given within 3 hours, yet some EMS systems still do not carry it. A colleague argues that since TXA does not directly stop bleeding, it is less important than mechanical hemorrhage control and should not be prioritized in a resource-limited EMS system. Critically evaluate this argument, considering the pathophysiology of traumatic coagulopathy, the evidence base, and the principles of damage-control resuscitation.

Show answer

Your colleague is correct that mechanical hemorrhage control is the first priority—no pharmacological agent can substitute for stopping the physical source of bleeding. However, the argument against TXA misunderstands the pathophysiology of traumatic hemorrhage and the principles of damage-control resuscitation. Trauma-induced coagulopathy (TIC) begins within minutes of injury due to tissue hypoperfusion and sympathetic activation, which triggers hyperfibrinolysis—the premature breakdown of clots that the body is trying to form. TXA, a lysine analog, inhibits plasminogen activation and thereby stabilizes clots, effectively making mechanical interventions more durable. The CRASH-2 trial (n > 20,000) demonstrated a statistically significant reduction in death due to bleeding (RR 0.85), with the greatest benefit when administered within the first hour (NNT ≈ 67). Importantly, TXA is inexpensive (approximately $5–10 per dose), has a long shelf life at room temperature, requires minimal training to administer, and has a favorable safety profile. From a damage-control resuscitation perspective, TXA directly combats one arm of the lethal triad (coagulopathy) and complements mechanical hemorrhage control rather than competing with it. In a resource-limited system, TXA arguably offers one of the highest value-per-dollar interventions available. The counterargument would be that the benefit is time-dependent and that delayed administration (> 3 hours) may actually increase mortality, so a system must ensure protocols allow for timely administration. Overall, TXA should be viewed as a pharmacological force multiplier for mechanical hemorrhage control, not a replacement.

SUMMARY

Hemorrhage Control & Traumatic Shock — Key Concepts

Summary

Hemorrhage is the leading preventable cause of trauma death. The four classes of hemorrhagic shock (I through IV) progress from compensated tachycardia with normal blood pressure to lethal cardiovascular collapse. The Shock Index (HR ÷ SBP) is a rapid bedside tool that detects occult hemorrhage before hypotension manifests, with values above 1.0 strongly predicting the need for massive transfusion. Prehospital hemorrhage control follows an anatomically driven algorithm: tourniquets for extremity hemorrhage, hemostatic wound packing and junctional devices for axillary, inguinal, and cervical bleeding, and rapid surgical transport for non-compressible truncal hemorrhage.

Resuscitation follows damage-control resuscitation principles: permissive hypotension (target SBP 80–90 mmHg), limited crystalloid, early blood products when available, and tranexamic acid (TXA) within three hours of injury. Throughout the resuscitation, the paramedic must actively combat the lethal triad of hypothermia, acidosis, and coagulopathy—a self-reinforcing cycle that accelerates hemorrhagic death. Hemorrhage control always precedes fluid resuscitation, and every intervention aims to bridge the patient to definitive surgical care.