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Bleeding

Bleeding, also known as hemorrhage, is the loss of blood from the circulatory system resulting from damage to blood vessels.^[1] It can manifest externally, such as through cuts or wounds on the skin, or internally, where blood accumulates within the body cavities or tissues, and may range from minor incidents like a small cut to severe, life-threatening events that lead to shock or organ failure.^[2]^[3] Bleeding is classified by the type of blood vessel affected, including arterial bleeding, which involves high-pressure spurting of bright red blood from arteries; venous bleeding, characterized by a steady flow of darker red blood from veins; and capillary bleeding, which appears as slow oozing from small surface vessels.^[3] Common causes encompass trauma or injury, surgical procedures, and underlying medical conditions such as blood clotting disorders (e.g., hemophilia or von Willebrand disease), cancers that erode vessels, peptic ulcers, liver or kidney failure, and use of anticoagulant medications like warfarin.^[1]^[4] Excessive alcohol consumption and postpartum complications can also precipitate significant hemorrhages.^[1]^[5] The management of bleeding prioritizes rapid control to prevent hypovolemic shock, involving direct pressure for external wounds, elevation, and tourniquets in severe cases, while internal bleeding often requires diagnostic imaging, surgical intervention, or blood transfusions.^[3] Early recognition of symptoms—such as rapid heartbeat, low blood pressure, pallor, or confusion in severe cases—is critical, as uncontrolled hemorrhage remains a leading cause of preventable death in trauma settings.^[6]^[3]

Physiology and Pathophysiology

Normal Hemostasis

Hemostasis is the physiological process that maintains blood in a fluid state within intact vessels while rapidly forming a localized hemostatic plug and clot at sites of vascular injury to prevent excessive blood loss. This process occurs in three main phases: vascular response, primary hemostasis (platelet plug formation), and secondary hemostasis (coagulation cascade), followed by fibrinolysis to restore normal blood flow.

Vascular Response

Upon vascular injury, the initial response involves immediate vasoconstriction of the damaged vessel, mediated by local reflexes, release of endothelium-derived vasoconstrictors such as endothelin, and stimulation of smooth muscle cells by neurotransmitters like serotonin and thromboxane A2 from platelets. This transient narrowing reduces blood flow to the injury site, minimizing blood loss within seconds to minutes. Simultaneously, the endothelium undergoes changes: intact endothelium normally expresses anticoagulants like thrombomodulin and heparan sulfate to inhibit clotting, but injury exposes subendothelial collagen and triggers endothelial cells to become procoagulant by expressing tissue factor (TF) and releasing von Willebrand factor (vWF). These alterations bridge the transition to platelet activation and coagulation.

Platelet Plug Formation

Primary hemostasis begins with platelet adhesion, where circulating platelets bind to exposed subendothelial collagen via glycoprotein Ib-IX-V receptors interacting with vWF, which is secreted from endothelial cells and Weibel-Palade bodies in response to injury. This adhesion is crucial under high shear stress conditions in arteries. Following adhesion, platelets activate through signaling pathways involving G-protein-coupled receptors stimulated by thrombin, ADP, and thromboxane A2, leading to shape change from discoid to spherical with pseudopods, granule release (alpha granules containing vWF, fibrinogen, and P-selectin; dense granules with ADP and serotonin), and expression of phospholipid surfaces (procoagulant activity). Activated platelets then undergo aggregation, mediated by glycoprotein IIb/IIIa (integrin αIIbβ3) receptors binding fibrinogen and vWF to form cross-links between platelets, creating a stable platelet plug that temporarily seals the breach. vWF plays a pivotal role in this process by facilitating initial tethering and supporting aggregation under flow. The plug formation typically occurs within 1-3 minutes, providing immediate hemostasis for small vessel injuries.

Coagulation Cascade

Secondary hemostasis reinforces the platelet plug through the coagulation cascade, a series of enzymatic reactions that culminate in fibrin clot formation. The cascade has two initiation pathways: the extrinsic (tissue factor) pathway and the intrinsic (contact activation) pathway, converging into a common pathway. In the extrinsic pathway, exposed tissue factor on subendothelial cells and activated platelets binds factor VIIa, forming the TF-VIIa complex that activates factor X to Xa in the presence of calcium and phospholipids. This pathway provides rapid initiation, amplifying the signal within seconds. The intrinsic pathway, slower and amplified by surface contact, involves factors XII, XI, IX, and VIII: factor XII activates to XIIa upon contact with collagen or polyphosphates from platelets, which then activates XI to XIa, IX to IXa (with VIIIa as cofactor), forming the tenase complex (IXa-VIIIa) that also activates factor X. Both pathways converge at the common pathway, where factor Xa, with cofactor Va on platelet surfaces, forms the prothrombinase complex that converts prothrombin (factor II) to thrombin (IIa). Thrombin then cleaves fibrinogen to fibrin monomers, which polymerize into a fibrin mesh stabilized by factor XIIIa cross-linking, encasing the platelet plug to form a durable clot. Thrombin also provides feedback amplification by activating factors V, VIII, XI, and platelets. Key deficiencies in these factors, such as fibrinogen or thrombin, can impair this process, though normal function ensures clot formation within 3-6 minutes.

Fibrinolysis

To prevent excessive clotting and restore vascular patency, fibrinolysis counterbalances hemostasis by degrading the fibrin clot once healing begins. Plasminogen, bound to fibrin, is converted to plasmin by tissue plasminogen activator (tPA) released from endothelial cells or urokinase plasminogen activator (uPA). Plasmin then proteolytically breaks down fibrin into soluble fragments (D-dimers), regulated by inhibitors like α2-antiplasmin and plasminogen activator inhibitor-1 (PAI-1) to ensure localized activity. This process typically starts hours after clot formation and completes over days, maintaining vascular integrity.

Sequence of Hemostasis Phases

The phases of hemostasis unfold sequentially:

Vascular spasm: Immediate vasoconstriction (seconds).
Platelet plug formation: Adhesion, activation, and aggregation (1-3 minutes).
Coagulation: Cascade activation leading to fibrin reinforcement (3-6 minutes).
Clot retraction and stabilization: Platelets contract the clot, and factor XIII cross-links fibrin (hours).
Fibrinolysis: Gradual clot dissolution (hours to days).

This orchestrated sequence ensures efficient bleeding control without compromising overall circulation.

Abnormal Bleeding Mechanisms

Abnormal bleeding mechanisms involve disruptions in the hemostatic balance that normally prevents excessive blood loss following vascular injury, leading to pathological hemorrhage through impaired clot formation or accelerated clot breakdown. These disruptions contrast with the coordinated steps of normal hemostasis, where vascular constriction, platelet plug formation, and fibrin stabilization maintain vascular integrity. Key categories include defects in vascular structure, platelet quantity or function, coagulation factor availability, fibrinolysis regulation, and anticoagulant system equilibrium.^[7] Vascular defects compromise the integrity of blood vessel walls, predisposing to rupture and uncontrolled bleeding even without significant trauma. Increased vessel fragility, as seen in connective tissue disorders like Ehlers-Danlos syndrome, results from weakened collagen support, causing easy bruising and spontaneous hemorrhage from minor stress. Structural abnormalities such as aneurysms—dilated, thinned arterial walls—or arteriovenous malformations, which are tangled networks of abnormal vessels bypassing capillaries, further heighten rupture risk due to hemodynamic stress and fragile endothelium. For instance, in brain arteriovenous malformations, these malformed vessels account for about 10% of subarachnoid hemorrhages, with bleeding triggered by high-pressure arterial flow against thin walls.^[8]^[9]^[10] Platelet disorders manifest as either quantitative reductions (thrombocytopenia) or qualitative dysfunctions, both impairing primary hemostasis by hindering platelet adhesion and aggregation at injury sites. Thrombocytopenia, defined as platelet counts below 150,000/μL, diminishes the availability of platelets for plug formation, leading to prolonged bleeding from mucosal surfaces and petechiae formation. Qualitative defects, such as in Glanzmann thrombasthenia—an inherited disorder caused by mutations in the ITGA2B or ITGB3 genes—prevent fibrinogen binding to the αIIbβ3 integrin receptor on platelets, resulting in absent aggregation despite normal platelet counts and morphology. This leads to severe mucocutaneous bleeding, including epistaxis and menorrhagia, often from childhood.^[7]^[11] Coagulation factor deficiencies interrupt the enzymatic amplification in the intrinsic, extrinsic, or common pathways of the coagulation cascade, failing to generate sufficient thrombin for stable fibrin clot formation. Hemophilia A (factor VIII deficiency) and hemophilia B (factor IX deficiency), both X-linked recessive disorders, predominantly affect the intrinsic pathway, causing delayed bleeding into joints and muscles due to inadequate fibrin stabilization. Vitamin K deficiency impairs γ-carboxylation of factors II, VII, IX, and X, as well as proteins C and S, reducing their activity and leading to prolonged prothrombin time; this is common in newborns or malabsorption states, resulting in easy bruising and intracranial hemorrhage if severe. These deficiencies collectively prolong clotting times and exacerbate bleeding from even trivial injuries.^[7]^[12] Fibrinolysis hyperactivity promotes premature degradation of fibrin clots through unchecked plasmin activity, tipping the balance toward excessive clot lysis and hemorrhage. Excessive plasmin generation, often from upregulated tissue plasminogen activator or urokinase plasminogen activator, overwhelms inhibitors like plasminogen activator inhibitor-1, leading to hyperfibrinolysis characterized by delayed post-traumatic bleeding or surgical oozing. Alpha-2-antiplasmin deficiency, a rare autosomal recessive disorder, specifically abolishes the primary physiological inhibitor of plasmin, allowing rapid fibrin breakdown and manifesting as severe hemorrhagic episodes, including hemarthroses and muscle hematomas, despite normal coagulation screening tests. This condition highlights how dysregulated fibrinolysis can cause bleeding independent of primary hemostasis defects.^[13]^[14] Anticoagulant effects contribute to abnormal bleeding when natural or therapeutic anticoagulant pathways become imbalanced, inhibiting clot formation beyond physiological needs. Therapeutic anticoagulants, such as warfarin or direct oral agents like rivaroxaban, can induce unchecked bleeding through overdose or supratherapeutic levels, suppressing factors II, VII, IX, and X or thrombin activity, respectively, and increasing risks of gastrointestinal or intracranial hemorrhage. For natural anticoagulants, severe deficiencies in protein C or S—vitamin K-dependent inhibitors of factors Va and VIIIa—paradoxically lead to consumptive coagulopathy in homozygous cases, where initial thrombosis depletes clotting factors, resulting in secondary bleeding tendencies like purpura fulminans in neonates. These imbalances underscore the narrow therapeutic window required to prevent both thrombosis and hemorrhage.^[15]^[16]

Types of Bleeding

By Location and Visibility

External bleeding refers to the loss of blood that occurs outside the body, typically visible through breaks in the skin or natural body openings.^[17] This type is directly observable, allowing for immediate assessment of the flow and volume.^[18] Common examples include lacerations from cuts or abrasions, epistaxis (nosebleeds), and gingival bleeding from the mouth.^[18] Characteristics of external bleeding often depend on the involved vessels, with arterial bleeding presenting as bright red blood in a pulsatile, spurting flow synchronized with the heartbeat, venous bleeding as a steady stream of darker red blood, and capillary bleeding as slow oozing from superficial wounds.^[3] These flow patterns can aid in rapid identification at the site of injury.^[19] Internal bleeding, in contrast, occurs within the body cavities, organs, or tissues, making it less visible and often requiring diagnostic imaging for confirmation.^[6] It can happen in various sites such as the gastrointestinal tract (leading to blood in stool or vomit), retroperitoneal space (around the kidneys and abdomen), or intracranial area (within the skull).^[20] Signs may include hematoma formation (localized swelling from blood pooling under the skin), organ distension (such as abdominal bloating from peritoneal bleeding), or visible indicators like bruising, petechiae, or blood emerging from orifices.^[21] The presentation of bleeding differs markedly by location: external bleeding often shows direct, observable flow that can pool externally, while internal bleeding leads to concealed accumulation, potentially causing pressure on surrounding structures without immediate visible loss.^[22] Pulsatile flows are more typical of exposed arterial sources in external cases, whereas internal bleeding tends toward steady or diffuse seepage, complicating timely detection.^[3] Specific risks associated with external bleeding include infection due to exposure of the wound to environmental contaminants.^[23] For internal bleeding, a primary concern is hypovolemia, where significant blood volume loss leads to circulatory shock, organ hypoperfusion, and potentially life-threatening complications if untreated.^[24]

By Vessel Involvement

Bleeding can be classified based on the type of blood vessel involved, which determines the pressure, flow pattern, color of the blood, and potential for rapid blood loss. This classification is crucial for understanding the urgency and characteristics of hemorrhage, as damage to different vessels leads to distinct clinical presentations. Arterial bleeding occurs when an artery is injured, resulting in high-pressure, pulsatile flow of bright red, oxygenated blood that spurts rhythmically with each heartbeat. This type is often the most severe due to the forceful ejection from the heart, making it difficult to control without immediate intervention; for example, rupture of the aorta can lead to massive, life-threatening hemorrhage into the mediastinum or pleural space.^[3]^[25] Venous bleeding involves damage to a vein, producing a steady, non-pulsatile flow of darker red, deoxygenated blood under lower pressure than arterial bleeding. Although less forceful, it can still result in significant volume loss, particularly from large veins; an example is the rupture of a varicose vein, which may cause profuse bleeding into surrounding tissues and, in rare cases, lead to exsanguination if not addressed promptly.^[3]^[26] Capillary bleeding arises from injury to the smallest blood vessels, characterized by slow oozing of blood with minimal volume and pressure, often appearing as minor seepage from the wound site. This type is typically the least severe and easiest to manage, as seen in conditions like petechiae, where broken capillaries cause pinpoint spots of discoloration on the skin due to leakage into surrounding tissues.^[3]^[27] Mixed or microvascular bleeding refers to diffuse hemorrhage involving small arteries, veins, and capillaries, often presenting as widespread purpura—non-blanchable purple discolorations from extravasation of blood into the skin or mucosa due to vessel wall fragility or dysfunction. This pattern lacks a single high-flow site and instead shows scattered involvement, as in thrombotic microangiopathies affecting small vessels.^[28] The implications for pressure and exsanguination risk vary markedly by vessel type: arterial injuries pose the highest risk of rapid, fatal blood loss due to systemic pressure (up to 120 mmHg systolic), potentially leading to shock within minutes; venous bleeding carries moderate risk with steady but voluminous flow (pressure around 10-15 mmHg), allowing more time for control but still capable of significant depletion; capillary and microvascular bleeding generally involves low pressure (<25 mmHg) and limited volume per site, reducing exsanguination threat unless widespread, though cumulative effects can contribute to anemia over time.^[3]^[29]

Causes of Bleeding

Traumatic Causes

Traumatic bleeding arises from physical injuries that disrupt vascular integrity, leading to hemorrhage that can range from minor external oozing to life-threatening internal blood loss. This type of bleeding is primarily induced by external forces such as motor vehicle accidents, falls, assaults, or penetrating injuries, distinguishing it from endogenous pathological processes. In trauma settings, uncontrolled bleeding accounts for approximately 30-40% of all trauma-related mortality, with rapid exsanguination occurring in the prehospital phase in up to 56% of fatal cases.^[30] The mechanisms of traumatic bleeding can be categorized into blunt force, penetrating, and shear injuries. Blunt force trauma, often from impacts like vehicle collisions or falls, causes compression and contusion of tissues, resulting in internal hemorrhage without skin breach; for instance, abdominal contusions may lead to organ lacerations and concealed bleeding.^[31] Penetrating trauma, such as stab wounds or gunshots, directly breaches vessels and organs, creating tracts that allow rapid blood escape, with high-velocity projectiles exacerbating damage through cavitation effects.^[32] Shear forces, typically from deceleration in accidents or rotational impacts, tear vessels and tissues along planes of stress, commonly associated with fractures that sever adjacent arteries or veins.^[33] These mechanisms often involve arteries, veins, and capillaries, with arterial bleeding presenting as pulsatile spurts and venous as steady flow.^[34] Common sites of traumatic bleeding include the head, abdomen, chest, pelvis, and extremities, where vascular-rich structures are vulnerable. In a large cohort of trauma patients, abdominal sources accounted for 44.3% of bleeding, followed by chest (20.4%), extremities (18.2%), and pelvis (11.4%).^[35] Head injuries frequently cause epidural or subdural hematomas, while abdominal trauma like splenic rupture can result in massive hemorrhage, potentially leading to hypovolemic shock.^[36] Extremity injuries, such as femoral fractures, may sequester significant blood loss into soft tissues or the thigh compartment.^[37] Severity of traumatic bleeding is influenced by several factors, including injury location, patient age, and comorbidities. Central injuries to the torso or head often prove more lethal due to proximity to vital organs and difficulty in external compression, whereas peripheral extremity bleeds may be more amenable to direct control.^[38] Older age exacerbates outcomes, as physiological reserves diminish, increasing susceptibility to coagulopathy and organ failure even with similar injury severity.^[39] Comorbidities, particularly pre-injury anticoagulation therapy, heighten bleeding risk by impairing hemostasis; for example, patients on anticoagulants experience increased risk of massive transfusion needs and higher mortality in trauma.^[40] Historically, trauma has been the leading cause of death from bleeding in individuals under 40-46 years old, with an estimated 31,000 preventable bleeding deaths annually in the United States alone, many from accidents or violence.^[41] In battlefield contexts, hemorrhage causes over 90% of potentially survivable deaths, as seen in conflicts from 2001-2011 where uncontrolled bleeding contributed to 24% of fatalities despite medical advances.^[42] These statistics underscore the persistent challenge of traumatic bleeding in both civilian and military settings.^[43]

Non-Traumatic Causes

Non-traumatic bleeding arises from underlying medical conditions, therapeutic interventions, infections, or toxins that disrupt normal hemostatic processes, leading to spontaneous or provoked hemorrhage without external injury. These causes often involve deficiencies in clotting factors, platelet dysfunction, or vascular fragility, resulting in manifestations such as petechiae, ecchymoses, or internal bleeding.^[7] Coagulopathies, including inherited disorders like hemophilia A and B, are characterized by deficiencies in clotting factors VIII and IX, respectively, which impair the formation of stable blood clots and predispose individuals to prolonged bleeding episodes, particularly into joints and muscles.^[44] Von Willebrand disease, another common hereditary coagulopathy, results from deficient or dysfunctional von Willebrand factor, leading to mucosal and cutaneous bleeding due to impaired platelet adhesion.^[7] Acquired coagulopathies, such as those from vitamin K deficiency or autoantibodies against clotting factors, can similarly cause excessive bleeding by neutralizing essential hemostatic components.^[45] Malignancies, particularly hematologic cancers like acute leukemia, frequently induce thrombocytopenia through bone marrow infiltration or chemotherapy effects, reducing platelet counts below critical thresholds and causing spontaneous mucocutaneous bleeding or severe hemorrhages.^[46] In leukemia, the resultant coagulopathy heightens the risk of life-threatening events, including intracranial or gastrointestinal bleeding, with incidence rates elevated in patients with platelet counts under 20 × 10^9/L.^[47] Solid tumors may also contribute via paraneoplastic syndromes or tumor invasion of vessels, though hematologic malignancies predominate in non-traumatic bleeding scenarios.^[48] Gastrointestinal conditions, such as peptic ulcers, can cause significant bleeding due to erosion of the mucosal lining and exposure of underlying vessels, often presenting as hematemesis or melena and requiring endoscopic intervention in severe cases.^[49] Organ failure, especially liver cirrhosis, compromises hemostasis by impairing the synthesis of clotting factors II, VII, IX, and X, alongside thrombocytopenia from splenic sequestration, resulting in prolonged prothrombin times and increased bleeding propensity, such as variceal hemorrhage.^[50] In advanced cirrhosis, this coagulopathy affects up to 70% of patients, manifesting as gastrointestinal bleeding or easy bruising, despite a rebalanced but fragile hemostatic system.^[51] Renal failure can exacerbate bleeding through uremic platelet dysfunction, further compounding risks in multi-organ dysfunction.^[52] Obstetric complications, notably postpartum hemorrhage, represent a major non-traumatic cause, often resulting from uterine atony, retained placenta, or trauma during delivery, leading to excessive vaginal bleeding that can rapidly progress to hypovolemic shock if not managed promptly.^[5] Iatrogenic causes stem from medical therapies or procedures that inadvertently provoke hemorrhage. Overuse or supratherapeutic dosing of anticoagulants like warfarin inhibits vitamin K-dependent factors, elevating the international normalized ratio (INR) and increasing the incidence of major bleeding events, including intracranial hemorrhage, by up to fivefold in atrial fibrillation patients.^[15] Direct oral anticoagulants, while generally safer, still carry a relative risk of gastrointestinal bleeding 1.25 times higher than vitamin K antagonists in some cohorts.^[53] Procedural complications, such as post-biopsy hemorrhage following liver or renal procedures, occur due to vessel disruption in friable tissues, with rates up to 5% in high-risk cases and often requiring embolization for control.^[54] Infections and toxins can trigger widespread coagulopathy leading to bleeding. Sepsis-induced disseminated intravascular coagulation (DIC) involves systemic activation of coagulation by inflammatory cytokines, consuming platelets and factors, which affects 30-50% of severe sepsis cases and doubles mortality through microvascular thrombosis and hemorrhage.^[55] Viral hemorrhagic fevers, exemplified by Ebola virus disease, disrupt endothelial integrity and coagulation via viral glycoproteins, causing petechiae, mucosal bleeding, and oozing from venipuncture sites in up to 50% of cases, though overt hemorrhage is not universal.^[56] Snake venoms from viper species induce venom-induced consumption coagulopathy (VICC) by activating prothrombin or degrading fibrinogen, leading to defibrination and prolonged bleeding from bite sites or systemic sites like the gastrointestinal tract, with risks persisting for days post-envenomation.^[57] Spontaneous bleeding risks are heightened in conditions like uncontrolled hypertension, where elevated blood pressure damages retinal vessels, resulting in retinal hemorrhages that appear as flame-shaped or dot-blot lesions and signal severe hypertensive retinopathy.^[58] These hemorrhages can occur without trauma, reflecting vascular fragility, and are associated with a heightened risk of hemorrhagic stroke, underscoring the need for blood pressure management to mitigate further bleeding.^[59]

Diagnosis

Clinical Evaluation

The clinical evaluation of a patient presenting with bleeding commences with a detailed history to characterize the episode, assess severity, and guide further assessment. Key elements include the onset of bleeding, which may be sudden in traumatic cases or insidious in non-traumatic ones, and its duration to determine acuity. The estimated amount of blood loss is quantified where possible, such as through patient reports of soaking through clothing or, in cases of vaginal bleeding, the number of saturated pads or tampons used. Associated symptoms are elicited, including dizziness, syncope, pallor, fatigue, abdominal pain, or changes in bowel habits, which can indicate hypovolemia or suggest the bleeding site, such as gastrointestinal involvement. A comprehensive physical examination follows to identify signs of active or recent bleeding and systemic effects. Vital signs are assessed first, with tachycardia and hypotension signaling significant volume loss and potential hemorrhagic shock. The skin and mucous membranes are inspected for pallor indicative of anemia, ecchymoses suggesting soft tissue hemorrhage, or petechiae pointing to platelet dysfunction or microvascular issues. In trauma or abdominal bleeding, the abdomen is palpated for tenderness, guarding, or masses that may denote internal hemorrhage or underlying pathology. Structured scoring systems aid in rapid prioritization during evaluation. In traumatic bleeding, the ABCDE approach systematically assesses airway, breathing, circulation (including hemorrhage control), disability, and exposure to identify life-threatening issues. For suspected intracranial bleeding, the Glasgow Coma Scale (GCS) evaluates consciousness through eye, verbal, and motor responses, with scores below 13 indicating potential severe injury requiring urgent intervention. Certain findings warrant immediate concern as red flags. Unequal pupils (anisocoria) may signal increased intracranial pressure from a bleed, such as uncal herniation, necessitating emergent evaluation. Observations during examination may align with external, visible bleeding or suggest concealed internal types.

Laboratory and Imaging Tests

Laboratory and imaging tests play a crucial role in confirming the source, extent, and underlying mechanisms of bleeding, providing objective data to guide further management beyond initial clinical assessment. These tests help quantify blood loss, evaluate hemostatic function, and identify anatomical abnormalities or vascular issues contributing to hemorrhage. Routine laboratory evaluations begin with a complete blood count (CBC), which assesses hemoglobin levels to detect acute drops indicative of significant blood loss and platelet counts to identify thrombocytopenia as a potential cause of bleeding. For instance, a hemoglobin level below 7 g/dL often signals substantial hemorrhage requiring intervention. Coagulation panels, including prothrombin time (PT) with international normalized ratio (INR), activated partial thromboplastin time (aPTT), and fibrinogen levels, evaluate the extrinsic, intrinsic, and common pathways of coagulation, respectively, to diagnose disorders like hemophilia or disseminated intravascular coagulation (DIC). Elevated D-dimer levels, a marker of fibrin degradation from fibrinolysis, can indicate hyperfibrinolysis or DIC in bleeding patients, though it is more commonly used to rule out thrombosis. Imaging modalities are selected based on suspected bleeding sites. The Focused Assessment with Sonography for Trauma (FAST) ultrasound rapidly detects free intraperitoneal fluid suggestive of hemoperitoneum in abdominal trauma, offering high specificity for clinically significant bleeding. Computed tomography (CT) scans, particularly non-contrast head CT, are the gold standard for diagnosing intracranial hemorrhage, revealing hyperdense lesions and guiding neurosurgical decisions. For gastrointestinal (GI) bleeding, CT angiography identifies active extravasation or vascular anomalies. Conventional angiography provides detailed vascular mapping and can localize obscure bleeding sources, often serving as both diagnostic and therapeutic in interventional settings. Specialized invasive tests are employed when initial evaluations suggest specific etiologies. Upper and lower endoscopy directly visualizes the GI tract to identify and sometimes treat sources like ulcers or varices, with high sensitivity for overt upper GI bleeding. Bone marrow biopsy is indicated for suspected hematologic causes, such as aplastic anemia or leukemia, allowing histological examination of marrow cellularity and morphology to confirm production defects leading to bleeding.

Classification

By Volume and Rate

Bleeding is classified by volume and rate to assess the physiological impact of blood loss, guiding initial evaluation in clinical settings. Volume refers to the percentage of total blood volume lost, while rate describes the speed of loss, influencing compensatory mechanisms and urgency of intervention. This classification, primarily based on the Advanced Trauma Life Support (ATLS) system, categorizes hemorrhage into four classes according to estimated blood loss in adults.^[60] Class I hemorrhage involves up to 15% of total blood volume loss, approximately 750 mL in a typical adult, resulting in minimal physiological changes such as slight tachycardia or no significant symptoms.^[60] Class II represents 15-30% loss (750-1,500 mL), leading to moderate tachycardia and narrowed pulse pressure due to early hypovolemia.^[60] Class III encompasses 30-40% loss (1,500-2,000 mL), marked by hypotension, marked tachycardia, and decreased urine output as perfusion to vital organs begins to impair.^[60] Class IV exceeds 40% loss (over 2,000 mL), causing profound hypotension, rapid weak pulse, and obtundation, posing immediate life-threatening risks to organ perfusion.^[60] The rate of bleeding further delineates its acuity: chronic bleeding occurs slowly over time, allowing partial compensation, as seen in gastrointestinal ulcers where ongoing low-volume loss may lead to anemia without acute instability.^[61] In contrast, acute bleeding is rapid and voluminous, overwhelming compensatory mechanisms quickly, exemplified by aortic dissection where sudden high-rate hemorrhage can cause rapid hemodynamic collapse. This distinction affects tissue perfusion, as even moderate volume loss at a high rate can precipitate shock faster than the same volume lost gradually. Total blood volume estimation forms the basis for these classifications, typically 70 mL/kg in adults, enabling calculation of absolute loss from percentage thresholds and assessment of perfusion deficits when losses exceed 15-20%, reducing cardiac output and oxygen delivery.^[62] Children exhibit lower tolerance to blood loss due to smaller absolute volumes (70-80 mL/kg) and higher baseline metabolic demands, where even 10-15% loss can impair perfusion more severely than in adults.^[63]

By Clinical Severity

Bleeding is classified by clinical severity according to its impact on patient symptoms, hemodynamic stability, organ function, and risk of mortality, providing a framework for risk stratification and management decisions. This approach focuses on physiological responses such as tachycardia, hypotension, and shock, rather than solely on blood loss volume. The Advanced Trauma Life Support (ATLS) program outlines four classes of hemorrhagic shock that align with this severity spectrum, correlating blood loss percentages with clinical manifestations.^[60] Mild bleeding is typically localized and self-limited, causing no significant hemodynamic changes or systemic effects. Examples include minor epistaxis or superficial cuts that stop spontaneously without intervention, with patients remaining asymptomatic or experiencing only minimal discomfort. In the ATLS classification, this corresponds to Class I hemorrhage, involving up to 15% of total blood volume (approximately 750 mL in adults), where vital signs are normal or minimally altered, and there is no evidence of organ hypoperfusion.^[60] Moderate bleeding produces noticeable symptoms but maintains overall stability, often requiring monitoring or supportive care without immediate life-threatening compromise. Patients may exhibit tachycardia, anxiety, or mild pallor, as seen in significant gastrointestinal bleeds that cause a heart rate increase but no hypotension. This aligns with ATLS Class II hemorrhage (15-30% blood volume loss, or 750-1,500 mL), where urine output decreases slightly, but mental status remains intact and peripheral perfusion is adequate.^[60] Severe or massive bleeding leads to profound hemodynamic instability, organ dysfunction, and high mortality risk, often progressing to hypovolemic shock. It is defined as blood loss at a rate exceeding 150 mL per minute, loss of 50% or more of total blood volume within 3 hours, or loss of one or more blood volumes within 24 hours, resulting in marked tachycardia, hypotension, oliguria, and altered mental status; in ATLS terms, this encompasses Classes III (30-40% loss, 1,500-2,000 mL) and IV (>40% loss, >2,000 mL), with profound shock and potential cardiovascular collapse.^[60]^[64] In specific contexts like postpartum hemorrhage, the World Health Organization (WHO) classifies severe cases as blood loss greater than 1,000 mL after delivery or any amount accompanied by signs of shock, contributing to over 20% of maternal deaths globally.^[60]^[65] While volume measurements contribute to assessing severity, clinical evaluation prioritizes these symptomatic and organ-level effects. Prognostic tools enhance severity assessment by quantifying risks of rebleeding and death. For upper gastrointestinal bleeding, the Rockall score integrates age, comorbidities, hemodynamic status, diagnosis, and endoscopic findings to predict outcomes, with scores of 5 or higher indicating a mortality risk exceeding 10%. Higher scores correlate with increased adverse events, guiding decisions on hospitalization and intervention. Special populations, such as the elderly, face amplified risks from bleeding of any severity due to reduced physiological reserve and comorbidities. In patients treated with warfarin, patients aged 80 years or older have a relative risk of severe bleeding complications 4.5 times higher than those under 50, with even moderate bleeds carrying elevated mortality from factors like frailty and polypharmacy.^[66] In geriatric cohorts, upper gastrointestinal bleeding mortality can reach 14-20%, underscoring the need for tailored risk stratification.^[67]

Management

Immediate Interventions

Immediate interventions for bleeding focus on rapidly stabilizing the patient by addressing life-threatening issues, particularly in cases of significant hemorrhage where circulatory collapse is imminent. The primary goal is to control blood loss, maintain vital organ perfusion, and prevent further deterioration until advanced care is available. These actions are guided by established protocols such as those from the Advanced Trauma Life Support (ATLS) framework, emphasizing a systematic approach to ensure airway patency, adequate breathing, and effective circulation.^[68] In managing acute bleeding, the ABCs—airway, breathing, and circulation—form the cornerstone of initial assessment and intervention, with circulation often prioritized in hemorrhagic scenarios to address exsanguination promptly. For airway, ensure it is open using basic maneuvers like head-tilt chin-lift if no cervical spine injury is suspected; for breathing, provide rescue breaths or ventilatory support if respiratory distress is present. Circulation takes precedence in bleeding patients, involving immediate hemostasis and volume support to counteract hypovolemia. This sequence, sometimes adapted as CABC (circulation-airway-breathing-circulation) in trauma with massive hemorrhage, has been shown to improve survival by focusing on bleeding control first.^[69]^[3] For external bleeding, the first-line technique is direct pressure applied firmly over the wound using a clean cloth or sterile gauze for at least five minutes to allow clot formation, as shorter durations may fail to achieve hemostasis. If direct pressure is insufficient, elevate the injured limb above heart level to reduce venous return and blood flow, provided no fracture is suspected. If bleeding persists, pack the wound with sterile gauze or a hemostatic dressing, applying direct pressure over the packing to promote clotting. Tourniquets are recommended for severe limb bleeding that cannot be controlled by pressure, placed 2-3 inches proximal to the wound on bare skin and tightened until bleeding stops; studies report up to 92% survival with proper application in prehospital settings, though conversion to pressure methods should occur within two hours under medical supervision to avoid complications.^[70]^[71]^[3]^[72] Patient positioning plays a supportive role in stabilizing hypovolemia; while the traditional Trendelenburg position (head down, legs elevated 15-30 degrees) was historically used to improve venous return, current evidence questions its efficacy and notes risks like aspiration, leading to preferences for passive leg raising as a reversible alternative that transiently increases preload without sustained hemodynamic benefits. In hypovolemic shock from bleeding, keep the patient supine with legs elevated if tolerated, and treat for shock by maintaining warmth and reassurance to mitigate compensatory mechanisms.^[73]^[74] Fluid resuscitation begins with establishing two large-bore intravenous lines (14-16 gauge) for rapid access, followed by an initial bolus of isotonic crystalloids such as normal saline or lactated Ringer's at 1-2 liters in adults to restore volume without delaying hemostasis. Over-resuscitation must be avoided to prevent dilutional coagulopathy and worsened bleeding; instead, adopt permissive hypotension in penetrating trauma or active hemorrhage, targeting a systolic blood pressure of 80-90 mmHg (or mean arterial pressure ≥65 mmHg) until surgical control is achieved, as aggressive normalization can dislodge clots and increase mortality.^[75]^[76] Supplemental oxygen is administered via high-flow mask (10-15 L/min) to achieve saturation of 94-98% in hypoxic patients, enhancing oxygen delivery to tissues amid reduced circulating volume. Continuous monitoring includes pulse oximetry for oxygenation, blood pressure via automated cuff or invasive arterial line if available, and heart rate to detect tachycardia indicative of ongoing loss; prehospital protocols also incorporate capnography for ventilation assurance and base deficit assessment to gauge shock severity. These measures, integral to protocols like those from the Committee on Tactical Combat Casualty Care (CoTCCC), facilitate early recognition of deterioration and guide transport to definitive care.^[77]^[3]

Advanced Treatments

Advanced treatments for bleeding focus on hospital-based interventions that target the underlying mechanisms of hemorrhage and promote hemostasis, often guided by the clinical severity of blood loss. Pharmacologic therapies play a central role in inhibiting fibrinolysis or reversing coagulopathies. Tranexamic acid, an antifibrinolytic agent, is administered intravenously to reduce bleeding in trauma and postpartum hemorrhage by blocking plasminogen activation, with a recommended dose of 1 g as soon as possible after onset, followed by an infusion.^[78] For anticoagulant-associated bleeding, vitamin K (5-10 mg IV) is used to reverse warfarin effects over 12-48 hours, while prothrombin complex concentrate (PCC) provides rapid correction of coagulation factors, achieving hemostatic levels within minutes and reducing mortality in intracranial hemorrhage.^[79] In hemophilia, factor concentrates—either plasma-derived or recombinant—are infused to replace deficient clotting factors VIII or IX, preventing or treating joint and muscle bleeds with dosing aimed at maintaining trough levels above 1-5%.^[80] Transfusion strategies restore volume and correct coagulopathy in severe cases. Packed red blood cells (RBCs) are transfused to replace lost oxygen-carrying capacity, typically targeting a hemoglobin of 7-9 g/dL in stable patients. Platelets and fresh frozen plasma (FFP) address thrombocytopenia and factor deficiencies, respectively. In massive transfusion protocols for ongoing hemorrhage exceeding 10 units of RBCs in 24 hours, a 1:1:1 ratio of RBCs, plasma, and platelets is employed to mimic whole blood and minimize dilutional coagulopathy, improving survival in trauma.^[81]^[82] Interventional radiology and endoscopy offer minimally invasive options for localized bleeding control. Transcatheter arterial embolization involves selective catheterization to deliver agents like coils or particles, occluding vessels in up to 90% of trauma cases while preserving organ perfusion. Endoscopic variceal ligation is the preferred method for esophageal varices, achieving initial hemostasis in 80-90% of acute bleeds, while sclerotherapy may be used as an alternative for esophageal or primary for gastric varices, injecting sclerosants to obliterate veins, though it carries risks like ulceration.^[83]^[84]^[85] Surgical interventions are indicated for uncontrolled massive hemorrhage unresponsive to less invasive measures. Vessel ligation ties off bleeding arteries, such as the internal iliac in pelvic trauma, to reduce pressure without complete ischemia. Packing with gauze or balloons tamponades diffuse oozing in the abdomen or pelvis, often as a damage-control step in unstable patients, followed by definitive repair once physiology stabilizes. Direct suturing or resection repairs lacerations in solid organs like the liver or spleen.^[86] Supportive care in the intensive care unit (ICU) ensures hemodynamic stability during advanced therapies. Continuous monitoring of vital signs, invasive pressures, and coagulation parameters guides adjustments, with vasopressors like norepinephrine used adjunctively in refractory hemorrhagic shock to maintain mean arterial pressure above 65 mmHg after volume resuscitation, though their role remains controversial due to potential vasoconstriction risks.^[87]

Etymology

The English word "bleeding" is the present participle of the verb "to bleed", which derives from Middle English "bleden", from Old English "blēdan" ("to bleed; to die"), from Proto-West Germanic "*blōdijan", from Proto-Germanic "*blōdijan" ("to smear with blood"), equivalent to "blōd" ("blood") + "-ijan" ("to make, cause to become"). It ultimately traces back to the Proto-Indo-European root "*bʰleh₃-" meaning "to bloom" or "to swell", reflected in the idea of blood bursting forth.^[88]^[89]

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