Blood loss: signs and first aid

Blood loss is a condition of circulating blood volume deficiency that occurs during acute bleeding, either external or internal. The danger is determined not only by the milliliters lost, but also by the rate of bleeding, coagulopathy, hypothermia, and acidosis: together, these form the "lethal triad" and quickly lead to shock. Clinically, these include weakness, cold sweat, tachycardia, a drop in blood pressure, shortness of breath, and confusion. However, with occult (internal) bleeding, there may be no external signs until sudden decompensation. Modern tactics emphasize early hemorrhage control and "damage control" rather than excessive crystalloids, which interfere with coagulation and increase blood loss. [1]

The internationally accepted staged classification of hemorrhagic shock (ATLS) is based on the percentage of blood volume loss and clinical features, ranging from class I (<15%) to class IV (>40%). It helps quickly assess severity and decide on immediate initiation of a massive hemorrhage protocol (MHP/MTP), laboratory activation, and operating room activation. Moreover, objective indicators (lactate, base deficit, pulse pressure dynamics) are often more accurate than blood pressure alone, especially in young patients. [2]

Individual scenarios – postpartum hemorrhage, gastrointestinal hemorrhage, intracranial and postoperative hemorrhage – have their own “subtleties”, but the core approach is the same: early identification, local hemostasis, coagulopathy antagonism (heat, calcium, fibrinogen/cryo, plasma and platelets), a restrictive red blood cell transfusion strategy and timely tranexamic acid. [3]

Modern protocols are also shifting toward low-titer whole blood (LWB) as an alternative to component therapy in severely injured patients, with a growing evidence base in civilian systems. At the same time, viscoelastic methods (ROTEM/TEG) are becoming routine, allowing for targeted correction of coagulation deficiencies (primarily fibrinogen). [4]

Code according to ICD-10 and ICD-11

Blood loss is coded based on the cause and location. In ICD-10, the general code for "Hemorrhage, not elsewhere classified" is R58, and for hypovolemic/hemorrhagic shock it is R57.1; for surgical complications, there are specific categories (e.g., I97.42 - intraoperative bleeding complicating another procedure on the circulatory organs). Traumatic and local sources (e.g., intracranial) are coded in the appropriate disease/injury chapters. [5]

ICD-11 uses a modular post-coordination system: a basic "stem" code, to which clusters with details (location, etiology, context) are added. For example, 8B0Z is "intracranial hemorrhage, unspecified," and ME24.9Z is "gastrointestinal bleeding, unspecified." For injuries, codes from the "Injury" section are added, along with expanders based on the nature of the injury. The official ICD-11 reference book is available online from the WHO. [6]

Correct coding is important for routing, surveillance, and payment: for hemorrhagic shock, code R57.1 (not "other shock") and specify the source of bleeding with maximum specificity, including traumatic and iatrogenic codes. This improves the comparability of outcomes and the quality of the data registry. [7]

In complex cases (e.g., a combination of head injury with subdural hematoma and coma), ICD-11 uses multiple codes, reflecting the type, location, and severity (GCS/loss of consciousness). This approach maintains analytical precision. [8]

Epidemiology

Acute hemorrhage remains the leading preventable cause of death from trauma in the working-age population. Death from exanguination predominates in the first 24 hours, hence the emphasis on early hemostatic strategies, including balanced transfusions and TXA. The PROPPR trial showed that a 1:1:1 (PPC:platelet:RBC) regimen reduced mortality specifically from blood loss in the first 24 hours compared with 1:1:2, although overall mortality was not different. [9]

In obstetrics, postpartum hemorrhage remains the leading cause of maternal mortality in many countries. The WOMAN trial convincingly demonstrated a reduction in mortality from bleeding when TXA was administered in the first 3 hours after birth; these findings formed the basis for WHO/FIGO recommendations. [10]

Gastrointestinal bleeding is one of the most common reasons for emergency hospitalization in adults; current ACG guidelines recommend a restrictive transfusion strategy (Hb threshold 7 g/dL) and early endoscopy within 24 hours. This has reduced blood overload and complications without worsening outcomes. [11]

In civilian traumatology, the use of low-titer anti-A/anti-B whole blood (LTOWB) is increasing; meta-analyses and registries demonstrate a reduction in 24-hour mortality and red blood cell requirements. The evidence base is expanding, and the safety profile is assessed as favorable when properly managed. [12]

Reasons

The etiology of blood loss is divided into traumatic (external/internal) and non-traumatic. Trauma—penetrating and blunt—causes bleeding from large vessels, parenchymal organs, pelvic bones, and long bones; the thoracic and abdominal cavities, as well as the retroperitoneal space, are particularly at risk. Rapid recognition of these "hidden" reservoirs determines the outcome. [13]

Non-traumatic causes are varied: gastrointestinal bleeding (ulcers, varicose veins, erosions), obstetric (uterine atony, ruptures, retained placenta), postoperative/iatrogenic, oncological, hemorrhagic strokes, coagulopathy, and anticoagulant therapy. For each scenario, there are specialized hemostasis algorithms (endoscopic, obstetric, neurosurgical, etc.). [14]

Medications increase blood loss: anticoagulants, antiplatelet agents, and some thrombolytics. Early reversibility is important (PCC for warfarin, specific antidotes for DOACs, platelets/desmopressin if indicated). Fibrinogen and platelet levels are also maintained. [15]

Physiological "factors"—hypothermia, acidosis, hypocalcemia—dramatically worsen bleeding, creating a "lethal spiral." Therefore, warming the patient and blood products, calcium correction, and early targeted coagulopathy are not options, but the basis. [16]

Risk factors

High rates of blood loss (arterial source, multiple injuries), anticoagulant therapy, liver failure, thrombocytopenia, and congenital coagulopathies increase the risk of severe outcomes. Elderly patients are less able to compensate for acute blood loss due to lower reserves and comorbidity. [17]

In trauma patients, risk factors for massive transfusion include hypotension and tachycardia on admission, cavity penetration, pelvic/femoral fractures, positive FAST ultrasound, high lactate and base deficit, and the need for early thoracotomy/laparotomy. These criteria are included in the MTP triggers. [18]

In obstetrics, the risk of PPC is increased by multiple pregnancies, large fetuses, prolonged labor, placenta previa/placenta accreta, and a history of uterine surgery. Early recognition and active management of the third stage of labor are key to prevention. [19]

For gastrointestinal bleeding, factors include NSAIDs, Helicobacter pylori, cirrhosis (portal hypertension), chronic renal failure, and anticoagulants. Risk stratification (e.g., GBS) and early endoscopy are helpful. [20]

Pathogenesis

Acute blood loss reduces venous return and stroke volume and activates the sympathetic nervous system: tachycardia and vasoconstriction attempt to maintain cardiac and cerebral perfusion. Losses of >30% of circulating blood volume lead to a drop in blood pressure and tissue hypoperfusion, increasing lactate and metabolic acidosis. Concurrently, the coagulation cascade is activated, but dilution by crystalloid factors and hypothermia shift the balance toward coagulopathy. [21]

Fibrinogen is the first declining factor in massive bleeding: levels <1.5 g/L are associated with increased blood loss. This is the basis for targeted recommendations to maintain fibrinogen ≥1.5-2.0 g/L with cryoprecipitate or concentrate and the use of ROTEM/TEG (FIBTEM) for personalized therapy. [22]

Antifibrinolytic protection with tranexamic acid reduces early mortality from bleeding if the drug is administered as early as possible (trauma - within the first 3 hours; obstetrics - also the sooner the better). Delayed administration in trauma is of no benefit. [23]

Citrate from blood components binds ionized calcium, causing hypocalcemia, which reduces myocardial contractility and coagulation; therefore, calcium is included in MTP protocols from the early stage (usually 1 g calcium chloride at the first units and then every ~4 units, with iCa monitoring). [24]

Symptoms

Classic symptoms include weakness, dizziness, nausea, cold, clammy skin, tachycardia, tachypnea, a drop in blood pressure, and oliguria. The severity of symptoms correlates with the shock class: in classes I-II, blood pressure may remain "normal" due to vasoconstriction, while pulse pressure narrows and heart rate increases. [25]

In case of external bleeding, the source is obvious (wound, bruises), in case of internal bleeding, there are indirect signs: pallor, pain/bloating, percussion/ultrasound signs of fluid, pain in the shoulder (diaphragmatic irritation), pelvic instability, neurological symptoms in case of intracranial bleeding. [26]

Obstetric hemorrhage is characterized by increased lochia, clots, uterine hypotension, and signs of shock; gastrointestinal hemorrhage is characterized by "coffee grounds," melena/hematochezia, weakness, and sometimes hypotension without obvious external losses. Postoperative hemorrhage is characterized by tachycardia, decreased hemoglobin levels, and blood-saturated drainage. [27]

Watch for “hidden” symptoms: increasing drowsiness/anxiety, decreased urine output <0.5 ml/kg/hour, cold extremities - early signs of decompensation even with maintained blood pressure. [28]

Forms and stages

The ATLS classifies hemorrhagic shock into four categories: I (<15% of circulating blood volume), II (15-30%), III (30-40%), and IV (>40%). As the class progresses, tachycardia and tachypnea intensify, pulse pressure narrows, blood pressure and urine output fall, and anxiety/stupor increases. This scale determines the severity of resuscitation and the need for MTP. [29]

By source, hemostasis is classified as external, internal (abdominal, parenchymal), and mixed; by etiology, it can be traumatic, obstetric, gastrointestinal, neurosurgical, or iatrogenic. Each type has its own hemostasis team and instruments (tourniquets and hemostatic dressings, endoscope, interventional X-ray, and operating room). [30]

By flow - massive (usually ≥4 units of red blood cells per hour/≥10 units per 24 hours) and non-massive; by coagulation - with coagulopathy (trauma-induced, anticoagulant-induced, liver) and without it. These "labels" help to more quickly call the correct sets of drugs/components. [31]

Postpartum hemorrhage (primary <24 hours, secondary 24 hours-6 weeks) and gastrointestinal bleeding (upper/lower) are classified separately. Each has its own routing and target thresholds/intervention timing. [32]

Complications and consequences

Immediate complications include hemorrhagic shock, multiple organ failure, myocardial/cerebral ischemia, and death from exanguination. Early complications include dilutional coagulopathy, hypothermia, acidosis, hypocalcemia, and the "death triad." These are prevented by restricting crystalloids, rewarming, and early hemostatic resuscitation. [33]

Transfusion complications include volume overload, hypocalcemia/hypomagnesemia (citrate), hypothermia, hyperkalemia, and rare immune reactions. MTP protocols include regular monitoring of ionized calcium, gases/lactate, and temperature management. [34]

Medium-term complications include thrombosis, infections, and multiple organ failure syndrome. The risk is reduced by using balanced components/whole blood, early correction of fibrinogen, and targeted antifibrinolytic therapy. [35]

In obstetrics - hysterectomy, fertility disorders, psychological consequences; early TXA and active management of the third stage of labor reduce mortality and disability. [36]

Diagnostics

The initial assessment follows the ABCDE algorithm: airway, breathing, circulation, neurological status, and exposure/examination. Concurrently, perform "compression control": direct pressure, tourniquets, and pelvic girdle. Important laboratory data in the first few minutes include Hb/hematocrit, lactate and blood gas composition, ionized calcium, platelets, PT/INR, APTT, and fibrinogen (preferably Clauss). [37]

Viscoelastic tests (ROTEM/TEG) provide a real-time picture of coagulation: coagulation onset, clot strength, and fibrinogen contribution (FIBTEM). This allows for a "smart" approach to administering cryoprecipitate/fibrinogen concentrate, plasma, or platelets, rather than "equally all." Guidelines recommend maintaining fibrinogen ≥1.5 g/L. [38]

Visualization: FAST ultrasound quickly identifies free fluid in the abdominal/pleural cavities; if stabilization occurs, whole-body CT is used to precisely localize the source. In obstetrics, clinical assessment of uterine tone and examination of the birth canal are recommended; in the gastrointestinal tract, early gastroscopy/colonoscopy (depending on the clinic) is recommended within the first 24 hours. [39]

When anticoagulating, assess the need for reversible treatment (PCC/vitamin K for warfarin; specific antidotes for dabigatran/factor Xa inhibitors) and target levels for resumption of anticoagulation after hemostasis.[40]

Table 1. Rapid diagnostic route for suspected massive bleeding

Step	What are we doing?	For what
Primary ABCDE	Control of the airway, breathing, and circulation	Reducing mortality during the "golden hour"
Field hemostasis	Pressure, tourniquet, pelvic bandage	Stopping an external source
Laboratory	Hb, gases/lactate, iCa, PT/INR, APTT, fibrinogen	Evaluation of shock and coagulopathy
Viscoelastic	ROTEM/TEG (including FIBTEM)	Targeted replacement therapy
Visualization	FAST/CT, endoscopy or obstetric examination	Finding and eliminating the source
[41]

Differential diagnosis

Not all hypotension and tachycardia are bleeding. It is important to distinguish from cardiogenic shock (infarction), obstructive shock (tamponade, pulmonary embolism, tension pneumothorax), sepsis, and anaphylaxis. Clues: jugular venous distension (tamponade), moist rales/ischemia (cardiogenic), wheezing/urticaria (anaphylaxis). If in doubt, perform a RUSH ultrasound in the emergency department. [42]

Internal bleeding is differentiated from other types of pain, including pancreatitis, perforation, aneurysm rupture, and ectopic pregnancy. FAST, CT, and Hb/lactate levels help prioritize. In obstetrics, coagulopathies (DIC), retained placenta, and cervical ruptures are excluded. [43]

Gastrointestinal bleeding is differentiated from esophageal emesis/Mallory-Weiss and nasal bleeding, which is swallowed and simulates "blood from the stomach." Early EGD and risk assessment (Glasgow-Blatchford) facilitate decisions on hospitalization and the timing of endoscopy. [44]

In pelvic trauma, distinguish between bleeding from the bony venous plexus (a bandage/tie is needed) and arterial bleeding (embolization/surgery). CT angio and the availability of an interventional radiologist are critical. [45]

Table 2. Blood loss or not? Key "forks"

Scenario	What does it look like?	How to distinguish/what to do
Hypotension + swollen veins	Tamponade/pulmonary embolism	Echo-ultrasound/CT-angio; do not inject crystalloids thoughtlessly
Abdominal pain + tachycardia	Pancreatitis/perforation/blood	FAST/CT; Hb/lactate; surgeon + endoscopy
Fainting in postpartum women	PPK, ICE	Uterine/rupture assessment; TXA + uterotonics
Melena vs. Swallowed Blood	Gastrointestinal tract vs. nose	Examination of the nasopharynx + EGDS
[46]

Treatment

1) Immediate measures. We stop bleeding ("compression control," tourniquet, hemostatic dressings, pelvic binder), minimize crystalloids, and activate MTP. We maintain the patient's temperature and blood product temperature. In parallel, we transport to the surgical site: operating room, endoscopy, angio-embolization. [47]

2) Balanced transfusion and/or whole blood. In trauma, the target approach is early blood products (plasma, platelets, red blood cells ≈1:1:1) or low-titer whole blood, which reduces death from exanguination. Platelets are not "last in line": early administration improves hemostasis. [48]

3) Antifibrinolytic therapy. Tranexamic acid: trauma - as early as possible, but no later than 3 hours (1 g bolus + 1 g infusion), reduces mortality from bleeding; obstetrics - 1 g as early as possible with PPC, repeat after 30 minutes if bleeding continues. Prophylactic use outside of clinical trials is not standard. [49]

4) Fibrinogen and targeted correction of coagulopathy. Maintain fibrinogen ≥1.5-2.0 g/L with cryoconcentrate; use ROTEM/TEG for dosing. In case of factor deficiency, plasma or PCC (especially in case of warfarin antagonism) are used. Maintain platelets >50×10⁹/L (higher - in case of TBI/neurosurgery). [50]

5) Calcium. Early correction of hypocalcemia is mandatory: calcium chloride 1 g at the first units of blood and then every ~4 units with monitoring of ionized calcium - recommendation of the Joint Trauma System and modern reviews. [51]

6) A restrictive red blood cell transfusion strategy (outside of active exanguinating bleeding). AABB 2023 recommends an Hb threshold of ≈7 g/dL for most hospitalized adults, with caveats for cardiac surgery/orthopedics/myocardial ischemia (7.5-8 g/dL). In gastrointestinal bleeding, ACG also supports a threshold of 7 g/dL in the absence of shock/ischemia. [52]

7) Specialized branches.

• Obstetrics: uterotonics (oxytocin/carbetocin), mechanical tamponade (balloon), TXA in the first 3 hours, surgical/endovascular hemostasis if ineffective. [53]
• Gastrointestinal tract: PPI, erythromycin before EGDS, endoscopic hemostasis, transfusion restrictions; for varicose veins - octreotide/terlipressin and ligation. [54]
• Pelvis/liver/spleen: pelvic traction, angio-embolization/surgery, packing with damage control. [55]

Table 3. When to activate the massive bleeding protocol (MTP)

Clinical triggers	Justification
Hypotension + tachycardia due to trauma/blood	Risk of shock class III-IV; blood products needed immediately
Positive FAST, CT with active extravation	The source of internal bleeding has been confirmed.
Need ≥4 units of red blood cells per 1 hour or prognosis ≥10 units/24 h	Classical criteria of "array"
Surgery/angio-embolization with ongoing bleeding	Ready-made containers with components/whole blood are required
[56]

Table 4. Tranexamic acid (TXA): where, when and how

Situation	Dose and time	What does it give?
Trauma with bleeding	1 g bolus as soon as possible + 1 g infusion; up to 3 hours	Reduction in death from bleeding
PPC (postpartum)	1 g IV slowly; repeat 1 g after 30 min if bleeding continues	Reducing maternal mortality
Prevention during childbirth	Considered in individual scenarios; not a "one size fits all" standard	Controversial data; refer to guidelines
[57]

Table 5. Fibrinogen and targeted coagulopathy

Parameter	Target	How do we replenish it?
Fibrinogen (Clauss)	≥1.5-2.0 g/l	Cryoprecipitate or fibrinogen concentrate
ROTEM FIBTEM A5/A10	Normalization by local references	Dose-dependent administration of concentrate/cryo
Platelets	>50×10⁹/l (higher in TBI)	Platelet concentrate
PT/INR, APTT	Correction during lengthening	Plasma/PCC as indicated
[58]

Table 6. Whole blood vs. component therapy (in trauma patients)

Approach	Potential benefits	Data
LTOWB (low titer whole blood)	Faster, more physiological factor/platelet ratio, less volume	Associated reduction in 24-hour mortality and red blood cell requirements
Balanced components (1:1:1)	Wide availability, flexibility	Reduction in death from exanguination vs 1:1:2 in the first 24 hours
Choosing a strategy	Depends on logistics and the blood bank	Recommendations from centers/systems, growing base
[59]

Table 7. Restrictive red blood cell transfusion (outside "active blood")

Scenario	Hb threshold (reference)	Source
Hospitalized adults	~7 g/dL	AABB 2023
Cardiac surgery/orthopedics/SVZ	7.5-8 g/dL	AABB 2023
Gastrointestinal bleeding without shock/ischemia	7 g/dL	ACG 2021
[60]

Prevention

Prevention of traumatic hemorrhage includes road and industrial safety, protective equipment, first aid training (pressure, tourniquet), and rapid evacuation. At the system level, this includes the availability of standardized MTPs, team training, regular simulations, access to ROTEM/TEG and whole blood/components. This directly contributes to reducing preventable mortality. [61]

Outside of trauma: NSAID and anticoagulant management (indications, doses, gastroprotection), H. pylori treatment, screening and correction of anemia, careful surgical technique and prevention of PPH (active management of the third stage of labor, access to uterotonics and TXA). Patient education on “red flags” (melena, hematemesis, postpartum hemorrhage) accelerates referral to help. [62]

Forecast

The prognosis for hemorrhage is critically dependent on the time to hemostasis and the quality of early resuscitation. The introduction of balanced transfusions/whole blood, early TXA, and targeted correction of coagulopathy reduce death from exanguination in the first 24 hours—the most dangerous period. Even in severe injuries, this strategy improves survival. [63]

In obstetrics, early TXA, uterotonics, and organized teamwork significantly reduce mortality; in the gastrointestinal tract, restrictive transfusion and early endoscopy reduce complications and hospitalizations. With a timely approach, most patients fully recover, but delayed recognition and uncontrolled coagulopathy worsen outcome. [64]

FAQ

• What are the dangers of “extra” crystalloids during blood loss?

They dilute coagulation factors and platelets, cool the patient, and exacerbate coagulopathy. Current protocols recommend rapid transition to blood products and targeted therapy. [65]

• Should everyone be given tranexamic acid?

No. Efficacy has been proven in trauma and postpartum hemorrhage if the drug is administered as early as possible (up to 3 hours); there is no benefit in trauma later than this. TXA is not used for general prophylaxis outside of research. [66]

• What is more important - whole blood or 1:1:1 scheme?

Both strategies are hemostatic. LTOWB shows advantages in some registries, and 1:1:1 in PROPPR reduced death from exanguination. The choice depends on logistics; the key is speed and balance. [67]

• What is the Hb threshold to use for transfusion?

In most adults, the threshold is approximately 7 g/dL outside of active, uncontrolled bleeding (AABB 2023). Exceptions include cardiac surgery/orthopedics and myocardial ischemia, where the threshold is higher. In gastrointestinal bleeding, the threshold is also 7 g/dL, unless there is shock/ischemia. [68]

• Why administer calcium in MTP?

Citrate from donor blood binds calcium, causing hypocalcemia, which impairs cardiac contraction and clotting. Therefore, calcium is administered early and regularly with monitoring of ionized calcium. [69]

Appendix: Classification of Hemorrhagic Shock (ATLS, Brief)

Class	Loss of blood volume	heart rate	BP/pulse pressure	Breath	Diuresis	Mental status
I	<15%	Normal/slightly ↑	Norm	14-20	>30 ml/h	Calm
II	15-30%	100-120	Norm/narrowing	20-24	20-30	Anxious
III	30-40%	120+	↓, expressing narrowing	24-35	5-15	Excited/stupor
IV	>40%	140+	Sharply ↓	>35	Minimum	Lethargy/coma
[70]