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Hematoma
Hematoma
Hematoma
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Hematoma
Other nameshaematoma
Contusion (bruise), a simple form of hematoma
SpecialtyEmergency medicine

A hematoma, also spelled haematoma, or blood suffusion is a localized bleeding outside of blood vessels, due to either disease or trauma including injury or surgery[1] and may involve blood continuing to seep from broken capillaries. A hematoma is benign and is initially in liquid form spread among the tissues including in sacs between tissues where it may coagulate and solidify before blood is reabsorbed into blood vessels. An ecchymosis is a hematoma of the skin larger than 10 mm.[2]

They may occur among and or within many areas such as skin and other organs, connective tissues, bone, joints and muscle.[3]

A collection of blood (or even a hemorrhage) may be aggravated by anticoagulant medication (blood thinner).[4] Blood seepage and collection of blood may occur if heparin is given via an intramuscular route; to avoid this, heparin must be given intravenously or subcutaneously.

Signs and symptoms

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Intramuscular hematoma development and progression on the vastus lateralis muscle from 6 hours after trauma to 86 hours

Some hematomas are visible under the surface of the skin (commonly called bruises) or possibly felt as masses or lumps. Lumps may be caused by the limitation of the blood to a sac, subcutaneous or intramuscular tissue space isolated by fascial planes. This is a anatomical feature that helps prevent injuries from causing massive blood loss. In most cases a hematoma as a sac of blood eventually dissolves; however, in some cases it may continue to grow due to blood seepage or show no change. If the sac of blood does not disappear, then it may need to be surgically cleaned out or repaired.

The slow process of reabsorption of hematomas can allow the broken down blood cells and hemoglobin pigment to move in the connective tissue. For example, a patient who injures the base of their thumb might cause a hematoma, which will slowly move all through their finger within a week. Gravity is the main determinant of this process.

Hematomas on articulations can reduce mobility of a member and present roughly the same symptoms as a fracture.

In most cases, movement and exercise of the affected muscle is the best way to introduce the collection back into the bloodstream.

Classification

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Types

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Intramuscular hematoma at buttocks as a result of a sports injury
Left to right: Epidural, subdural, and intracranial hematoma of the brain
Hematoma of the ankle caused by a 3rd degree sprain

Degrees

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  • Petechiae – small pinpoint hematomas less than 3 mm in diameter;
  • Purpura (purple) – a bruise about 3-10 mm in diameter, generally round in shape;
  • Ecchymosis – subcutaneous extravasation of blood in a thin layer under the skin, i.e. bruising, over 1 cm in diameter.[8]

Etymology

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The English word "hematoma" came into use in 1826. The word derives from the Greek αἷμα haima "blood" and -ωμα -oma, a suffix forming nouns indicating a mass or tumor.[9]

See also

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Hematoma

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from Grokipedia
A hematoma is a localized collection of outside the normal confines of vessels, occurring in an extravascular space due to rupture or damage of a vascular structure, which allows to accumulate and often clot in surrounding tissues, organs, or body cavities. This condition differs from active hemorrhage by the formation of a contained clot, which the body may gradually reabsorb, though the process and outcomes vary by size, location, and underlying factors. Hematomas can range from minor, self-resolving bruises to life-threatening accumulations that compress vital structures, such as those within the . Hematomas are classified primarily by their anatomical location, which influences symptoms, severity, and . Common types include subcutaneous hematomas (under the skin, appearing as raised, discolored swellings), intramuscular hematomas (within muscle tissue, often from direct trauma), and organ-specific variants like splenic or hepatic hematomas following abdominal . More critical forms occur internally, such as intracranial hematomas, which encompass epidural (between the skull and ), subdural (between the dura and brain surface), and intracerebral (within brain tissue) subtypes, potentially causing increased and neurological deficits. Other notable types include subungual (under the nail bed), auricular (in the ), and retroperitoneal (in the space behind the ), each presenting unique risks like or . The primary cause of hematomas is trauma, such as blunt force from falls, accidents, or , which damages vessel walls and leads to of . Iatrogenic factors, including surgical procedures, biopsies, or injections, as well as medications (e.g., or aspirin) that impair clotting, significantly increase risk by promoting uncontrolled bleeding. Spontaneous hematomas may arise in patients with coagulopathies, , hemophilia, or , without evident injury, particularly in vulnerable sites like the or . Risk factors encompass advanced age, therapy, underlying coagulopathies, and trauma-prone activities without protective gear, with older adults being especially prone to subdural types from minor head impacts. Symptoms depend on the hematoma's location and size but commonly include localized pain, swelling, tenderness, warmth, and bruising (ecchymosis) for superficial cases. Internal hematomas may manifest subtly or emergently: abdominal ones with hypotension, tachycardia, or abdominal distension; intracranial with progressive headache, confusion, vomiting, seizures, focal weakness, or coma due to brain compression. Diagnosis typically involves physical examination, patient history, and imaging—ultrasound for superficial or abdominal sites, CT or MRI scans for intracranial evaluation—to confirm the extent of bleeding and rule out active hemorrhage. Blood tests, such as complete blood count and coagulation studies, assess for underlying coagulopathy. Treatment strategies prioritize stabilization and depend on severity: small, asymptomatic hematomas often resolve conservatively with rest, ice application, compression, elevation ( protocol), and over-the-counter pain relief (avoiding antiplatelet agents). For larger or symptomatic cases, interventions include reversing anticoagulation (e.g., with or ), percutaneous drainage, or embolization via to stop bleeding sources. Surgical options, such as for intracranial hematomas or for abdominal ones, are reserved for those causing hemodynamic instability, organ compromise, or neurological deterioration, with monitoring in intensive care as needed. Complications like , re-bleeding, or can occur, but most hematomas heal within weeks to months, though intracranial cases may require long-term rehabilitation for residual deficits.

Definition and Pathophysiology

Definition

A hematoma is defined as a localized collection of extravasated outside the s, trapped within an organ, tissue space, or , typically resulting from the rupture of a and forming a clotted mass. This accumulation occurs when leaks from damaged vasculature and is contained by surrounding tissues, preventing free drainage. Key characteristics of a hematoma include its tendency to clot due to activation of the coagulation cascade, distinguishing it from active hemorrhage, which involves ongoing, diffuse bleeding without localization. Over time, the clotted blood may become organized and encapsulated by a fibrous pseudocapsule formed through inflammatory and reparative processes in the surrounding tissue. Unlike ecchymosis, which is a superficial, flat discoloration from leakage without significant formation or tissue displacement, a hematoma often creates a palpable due to involvement of larger vessels. The formation of a hematoma presupposes a breach in blood vessel integrity, where normal hemostatic mechanisms—such as , formation, and clot stabilization—fail to fully contain the , allowing blood to pool in a confined area. This failure disrupts the balance that maintains blood within the vascular system under physiological conditions.

Pathophysiology

A hematoma forms when a is injured, leading to of into surrounding tissues or potential spaces, where it accumulates as a localized collection outside the vascular system. This initial phase involves the escape of liquid , which is influenced by the vessel's size, local , and the of surrounding tissue barriers. If hemostatic mechanisms fail to fully contain the bleed, the accumulation persists and expands, driven by factors such as hydrostatic gradients favoring outward flow and incomplete vessel or . Hemostasis plays a central role in attempting to limit hematoma expansion through primary and secondary processes. Platelet aggregation occurs first upon exposure to subendothelial , forming a temporary plug that adheres via and activates further platelet recruitment. This is reinforced by the coagulation cascade, where the extrinsic pathway is rapidly initiated by exposure, activating factor VII to VIIa, while the intrinsic pathway is triggered by contact activation of , involving factors XI, IX, and VIII. Both pathways converge at activation, leading to prothrombin conversion to , which cleaves fibrinogen into strands that stabilize the clot; , mediated by , later balances this by degrading to prevent excessive but can contribute to hematoma persistence if dysregulated. The tissue response to the hematoma begins with an acute inflammatory phase, where the clot releases cytokines such as tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) from infiltrating macrophages and T cells, recruiting additional immune cells to clear debris and initiate repair. Fibroblasts then infiltrate the organizing clot, depositing components like and hyaluronan to form , eventually leading to and encapsulation. In chronic hematomas, incomplete resolution may result in due to ongoing , converting solid clot to a serous or semi-liquid state, or from prolonged exposure of necrotic tissue to calcium. In enclosed compartments, such as the , hematoma expansion alters local dynamics, with limited tissue compliance causing exponential rises in pressure that compress surrounding structures and impair .

Causes

Traumatic Causes

Traumatic hematomas arise from physical injuries that disrupt vessels, leading to localized accumulation outside the vascular system. These injuries typically involve mechanical forces that damage vessel walls, triggering the pathophysiological clotting response where platelets aggregate and forms to stem , though the extent of hematoma formation depends on the injury's severity and location. Blunt force trauma is a primary mechanism, often resulting from direct impact that compresses tissues and ruptures capillaries or small vessels without penetration. For instance, contusions from falls or blows can cause intramuscular hematomas, where pools within muscle compartments, leading to swelling and . Such injuries are common in contact sports or accidents, with the force causing shearing of muscle fibers and associated vasculature. Penetrating injuries, such as those from stab wounds or gunshot projectiles, directly lacerate blood vessels, promoting rapid hematoma formation in affected areas. A notable example is epidural hematomas, which frequently stem from fractures that tear the , allowing blood to accumulate between the and ; these often occur in high-velocity impacts like motor vehicle collisions. Approximately 75% of epidural hematomas involve an associated fracture from such penetrating or severe . Shear forces, generated by rapid deceleration or twisting motions, can tear vessels at fixed anatomical points, contributing to hematomas in deeper structures. In cases of from blunt chest trauma, such as in high-speed crashes, on the aortic wall may lead to retroperitoneal hematomas as blood leaks into the surrounding space. These forces are particularly relevant in accidents, where the aorta's suspension between fixed and mobile segments amplifies injury risk. Specific risk factors for traumatic hematomas include participation in high-impact activities like (e.g., football or ) or involvement in accidents such as falls from heights or vehicular crashes, which increase exposure to blunt or penetrating forces. A common peripheral example is subungual hematomas from nail bed crush injuries, often seen in hammer strikes or door slams, where pressure disrupts subungual vessels and causes blood to collect under the nail plate. Epidemiologically, traumatic hematomas are prevalent in blunt abdominal trauma scenarios, particularly motor vehicle accidents, which account for a significant portion of cases. For example, occur in up to 45% of patients with , representing about one-third of all solid organ injuries in such events, often due to deceleration forces impacting the spleen against the diaphragm or spine.

Non-Traumatic Causes

Non-traumatic hematomas develop due to intrinsic disruptions in or vessel integrity, often stemming from underlying medical conditions or therapeutic interventions, rather than external forces. These occurrences are less common than traumatic hematomas but can be life-threatening, particularly in enclosed spaces like the retroperitoneum or cranium, where rapid expansion may lead to organ compression. Coagulation disorders significantly predispose individuals to spontaneous hematomas by impairing the blood's ability to form clots. Hemophilia A, caused by deficiency, and hemophilia B, due to deficiency, frequently result in deep tissue hematomas, such as intramuscular or joint bleeds, even without provocation, due to fragile vessel walls and prolonged bleeding tendencies. (vWD), the most common inherited bleeding disorder, involves deficient or dysfunctional , leading to mucosal and soft tissue hematomas, including rare iliopsoas muscle hemorrhages that mimic acute abdominal emergencies. Anticoagulant therapy exacerbates these risks; for instance, use can induce spontaneous retroperitoneal hematomas through excessive anticoagulation, often presenting with flank pain and hemodynamic instability with an incidence of 0.6%-6.6% in patients on therapeutic anticoagulation. Vascular pathologies contribute to non-traumatic hematomas by creating fragile or abnormal blood vessels prone to rupture. can cause spontaneous hematomas, particularly intracerebral ones, by chronically damaging small vessel walls and leading to rupture without trauma. Cerebral aneurysms, particularly those in the , may leak or burst, causing pure acute subdural hematomas without , as seen in cases where aneurysmal rupture leads to localized blood accumulation. Arteriovenous malformations (AVMs), tangled networks of arteries and veins lacking intervening capillaries, heighten hemorrhage risk due to high-flow shunting and vessel wall stress, commonly resulting in intracranial or spinal hematomas. , an inflammatory condition affecting vessel walls, weakens structural integrity and can precipitate hematomas in affected organs, such as deep intracerebral bleeds from associated aneurysms or occlusive changes. Iatrogenic hematomas arise from medical procedures that inadvertently damage vessels, occurring without external trauma but as a direct consequence of intervention. Renal biopsies frequently cause perirenal hematomas due to needle-induced vascular , with rates up to 90% in some series, though most are and resolve conservatively. Similarly, central venous catheterizations can lead to retroperitoneal or mediastinal hematomas from arterial puncture, particularly when guidance is absent, resulting in significant morbidity in anticoagulated patients. core biopsies, while generally safe, occasionally produce pseudoaneurysms or expanding hematomas from vascular trauma, necessitating in severe cases. Rare spontaneous intramural duodenal hematomas have been linked to , where enzymatic degradation of vessel walls in the inflamed triggers bleeding and obstruction, often requiring endoscopic or surgical intervention. In vulnerable populations with these predispositions, non-traumatic hematomas carry risks of expansion and secondary complications like .

Clinical Presentation

Signs and Symptoms

Hematomas typically present with localized , which may feel throbbing or pressure-like due to the accumulation of exerting force on surrounding tissues. Swelling occurs as the pooled causes by displacing adjacent muscles or . The affected area is often tender to touch, and in superficial hematomas, it may feel raised with a spongy, rubbery, or lumpy texture due to the pooled and clotted blood, distinguishing it from flat bruises (ecchymoses). Visible discoloration develops, progressing from initial redness to or within hours to days, then to green, yellow, or brown as the body breaks down the over 1–2 weeks. Symptoms vary by hematoma location. In intracranial cases, patients commonly experience severe , , , drowsiness, unequal pupil sizes, slurred speech, and neurological deficits such as or on the side opposite the injury. For extremity hematomas, reduced mobility results from pain and stiffness, and signs of may include , numbness, or intense pain on passive movement. The temporal progression of symptoms differs between acute and chronic hematomas. Acute hematomas develop rapidly after , with immediate onset of , swelling, and localized tenderness. Chronic hematomas expand gradually over days to weeks, potentially leading to subtler symptoms like persistent fatigue or from ongoing blood loss, as seen in large retroperitoneal or expanding collections.

Complications

Hematomas can lead to various local complications due to the accumulation of and subsequent pressure on surrounding tissues. One common local effect is , which may result in formation if the hematoma becomes a nidus for , particularly in cases involving breaches or underlying immunocompromise. Tissue can occur from prolonged compression by the expanding hematoma, impairing supply to adjacent structures and leading to ischemia and . Additionally, chronic unresolved hematomas may promote , where organized products and inflammatory responses cause formation, potentially resulting in contractures that limit joint mobility and function. On a systemic level, large-volume hematomas pose risks such as , arising from significant blood loss that depletes circulating volume and impairs organ perfusion. In massive cases, particularly those associated with coagulopathies or obstetric complications, hematomas can trigger (DIC), a disorder characterized by widespread clotting and bleeding due to consumption of factors. Specific complications vary by hematoma location. Intracranial hematomas, for instance, can cause by exerting on neural structures, leading to brainstem compression, altered consciousness, and potentially fatal outcomes if untreated. Retroperitoneal hematomas often result in organ compression, such as ureteral obstruction that impairs kidney function and may progress to acute renal failure through and reduced glomerular filtration.

Diagnosis

Physical Examination

The physical examination for a hematoma begins with a systematic assessment to identify localized blood accumulation and its effects on surrounding structures, correlating with reported symptoms such as or swelling. This bedside evaluation is crucial for initial and guiding further management, focusing on non-invasive techniques to detect abnormalities without relying on imaging. Inspection involves visual evaluation of the affected area for signs of ecchymosis, which appears as bluish-purple discoloration due to extravascular blood leakage into the skin, often expanding over time. Asymmetry or visible may be evident, such as bulging in the or limb swelling that distorts normal contours. In cases of superficial hematomas, skin changes like petechiae or can indicate smaller vessel involvement. Palpation follows inspection, gently assessing the site for fluctuance, a fluid-like wave suggestive of liquefied in superficial collections, though this may be absent in deeper hematomas. The area often feels warm due to acute from breakdown products and is tender to touch, with firmness indicating organized clot formation. Hematomas may also feel spongy, rubbery, or lumpy upon palpation, distinguishing them from typical flat ecchymoses (bruises), which lack a raised or mass-like texture. , a crackling sensation, may occur if the hematoma overlies a with air or tissue disruption. Functional tests evaluate the hematoma's impact on nearby structures, including range of motion to detect stiffness or pain-limited movement in extremities. Neurovascular status is assessed by checking distal pulses for adequacy, sensation for paresthesia, and motor function for weakness, using the 6 Ps (pain, pallor, paresthesia, paralysis, poikilothermia, pulselessness) as a framework, particularly in limb hematomas. Vital signs are monitored for hemodynamic instability, such as tachycardia or hypotension signaling significant blood loss. Special maneuvers aid in specific locations; for abdominal hematomas, ballotment—pushing the mass to assess mobility—or the Fothergill sign, where the mass remains palpable and unchanged during rectus contraction, helps localize it to the sheath without crossing the midline. In suspected ocular or orbital involvement, fundoscopy examines the for hemorrhage or , revealing indirect effects of increased from associated hematomas.

Imaging and Laboratory Tests

Imaging modalities play a crucial role in confirming the presence, location, and extent of hematomas, guiding treatment decisions based on the suspected site and acuity. Ultrasound is particularly useful for evaluating superficial and soft tissue hematomas, where it reveals hypoechoic or heterogeneous fluid collections with high sensitivity (approximately 80-96%). Color Doppler ultrasound enhances this assessment by detecting vascular involvement, such as pseudoaneurysms or active bleeding, with sensitivity and specificity exceeding 95% in stable patients with extremity trauma. Computed tomography (CT) serves as the gold standard for diagnosing intracranial and abdominal hematomas due to its rapid acquisition and ability to detect active bleeding through contrast extravasation, offering nearly 100% for acute cases. In intracranial settings, non-contrast CT identifies hyperdense crescent-shaped collections in acute subdural hematomas, while contrast-enhanced studies highlight ongoing hemorrhage. However, CT's exposure poses limitations, particularly in pediatric patients, where cumulative doses from head CT scans may elevate the risk of hematological malignancies by 1-2 cases per 10,000 scans at mean doses of 8 mGy. Magnetic resonance imaging (MRI) excels in characterizing chronic or spinal hematomas, staging blood products by signal intensity variations—such as high T1 and T2 signals persisting up to 10 months in resolving collections—and providing superior contrast without . It is the preferred modality for evaluating muscle hematomas or masses persisting beyond one month, delineating borders, , and fascial involvement. Laboratory tests complement imaging by assessing the systemic impact of blood loss and underlying . A (CBC) evaluates from hemorrhage, with or declining in cases of significant blood loss, necessitating serial monitoring for transfusion needs. panels, including (PT), activated partial thromboplastin time (aPTT), and international normalized ratio (INR), identify bleeding diatheses, especially in anticoagulated patients, where abnormalities increase complication risks. Type and crossmatch testing prepares for potential transfusions in significant hematomas.

Classification

By Location

Hematomas are classified by their anatomical location, which influences their , potential complications, and considerations. This classification highlights how the site of blood accumulation affects surrounding structures, with superficial hematomas often being more accessible for observation or drainage, while deep or enclosed hematomas pose greater risks due to buildup or organ involvement. Subcutaneous hematomas, the most common type, occur under the skin and are frequently visible as bruises resulting from minor trauma or procedures such as injections, particularly in patients on anticoagulants. These collections typically involve small vessels and resolve spontaneously but can cause localized swelling and discoloration. Intramuscular hematomas develop within muscle tissue, often following direct trauma or strain, leading to significant pain due to pressure on muscle fibers and potential compression. They carry a risk of myonecrosis, where muscle tissue occurs from ischemia, and are commonly seen in the or extremities. Intracranial hematomas, located within the skull, include subtypes such as subdural (between the dura and brain), epidural (between the dura and skull), and intraparenchymal (within brain tissue), each with varying degrees of urgency based on expansion rate and mass effect. The confined cranial space amplifies risks of increased intracranial pressure, potentially leading to herniation. Subdural hematomas are particularly common in the elderly due to falls, as age-related brain atrophy stretches bridging veins, making them prone to rupture. Visceral hematomas arise within organs, such as hepatic or splenic in the context of , where blunt force can cause parenchymal without immediate capsular rupture. These often present with hemodynamic instability if significant blood loss occurs. Subungual hematomas form under the nail bed, typically from trauma such as a slammed , causing intense and visible discoloration under the nail; they may require trephination for relief if large. Retroperitoneal hematomas occur in the space behind the , often spontaneously in patients on anticoagulants or with vascular rupture, leading to , , and potential femoral neuropathy if involving the . Auricular hematomas, though less common, occur in the external , frequently in contact sports like due to repetitive separating from cartilage. Overall, location determines accessibility for intervention, with superficial sites allowing easier monitoring compared to deep or enclosed areas like the cranium, where even small volumes can cause disproportionate harm.

By Severity

Hematomas are categorized by severity according to their size, expansion rate, symptomatic impact, and potential to cause hemodynamic instability or , guiding clinical decision-making despite the absence of a universal grading system. Severity assessment often relies on organ-specific scales or broader hemorrhage classifications, emphasizing clinical gravity over anatomical site. For instance, the American Association for the Surgery of Trauma (AAST) Organ Injury Scale for splenic hematomas grades injuries from I (mild, subcapsular hematoma <10% surface area, non-expanding) to V (severe, shattered spleen with hilar vascular injury and >25% devascularization), correlating higher grades with increased risk of rupture and need for intervention. Similarly, for intracerebral hematomas, the Intracerebral Hemorrhage (ICH) score assigns points based on factors including hematoma volume (>30 mL as a marker of severity), Glasgow Coma Scale (3-12 indicating moderate to severe impairment), infratentorial origin, , and age ≥80 years, with total scores of 0-1 denoting low mortality risk (mild) and ≥3 high risk (severe). Key factors influencing severity include the rate of expansion, which elevates risk when ongoing bleeding occurs, as seen in up to 38% of ICH cases presenting within 6 hours and leading to worse outcomes. Comorbidities such as anticoagulation therapy exacerbate severity by promoting expansion; patients with VKA-associated ICH experience hematoma growth in approximately 36% of cases compared to 19% without, often resulting in higher mortality. Volume thresholds further define criticality, with estimated blood loss exceeding 20-30% of total (Class III or IV in ATLS hemorrhage classification) signaling severe compromise, including , , and . Outcome correlations vary by grade: mild hematomas, typically small (<20-30 mL in ICH or Class I/II blood loss), frequently resolve spontaneously through reabsorption, as documented in asymptomatic chronic subdural cases with low-density collections. In contrast, severe hematomas (>10 cm equivalent or expanding, akin to AAST grade IV-V or ICH score ≥4) correlate with poor , including 70-90% mortality in high-volume ICH, often requiring aggressive intervention to mitigate risks like or multi-organ failure. The clinical manifestation of severity remains influenced by location, but grading prioritizes intrinsic expansion and volume dynamics.

Management

Conservative Management

Conservative management of hematomas focuses on supportive measures to promote natural resolution while minimizing risks of further bleeding or complications, particularly in stable, non-life-threatening cases. For extremity hematomas, the RICE protocol—rest, ice, compression, and elevation—is a foundational approach to reduce swelling, pain, and bleeding in soft tissues. Rest involves immobilizing the affected area to prevent aggravation, ice application (typically 15-20 minutes every few hours) constricts blood vessels to limit hematoma expansion, compression with elastic bandages controls hemorrhage without excessive pressure, and elevation above heart level facilitates venous drainage. This protocol is especially applicable to superficial or muscular hematomas in athletes or trauma patients, where it supports healing without invasive intervention. It is not safe to puncture or drain a hematoma yourself, particularly in the hand, as this can cause infections, further complications such as compartment syndrome, or tissue damage. Standard conservative treatment for extremity hematomas includes the RICE method along with pain relief as needed. Medical attention should be sought if the hematoma is large, very painful, growing, or shows signs of infection or compartment syndrome. In stable cases across various locations, such as small intracranial or abdominal hematomas without neurological deficits or hemodynamic instability, close observation with serial clinical examinations is recommended to track progression. These exams assess for changes in size, tenderness, or functional impairment, often complemented by repeat imaging if initial scans show minimal volume. Conservative approaches are typically selected for hematomas classified as mild to moderate in severity, where active bleeding has ceased, and align with guidelines such as the 2022 AHA/ASA recommendations, emphasizing blood pressure control (systolic <140 mm Hg if feasible) to minimize expansion risk. Pharmacological interventions play a supportive role, emphasizing pain control and addressing underlying coagulopathy. Analgesics like acetaminophen are preferred for symptom relief, while nonsteroidal anti-inflammatory drugs (NSAIDs) should be used cautiously due to their potential to impair platelet function and exacerbate bleeding risk. For patients on anticoagulants, prompt reversal is essential; vitamin K and prothrombin complex concentrates are administered for warfarin-associated hematomas to restore hemostasis. Ongoing monitoring is critical to detect deterioration and guide escalation. Vital signs, including blood pressure and heart rate, are tracked frequently to identify hypovolemia or shock, while serial hemoglobin levels help gauge ongoing blood loss. Indications for transitioning from conservative care include significant hematoma expansion (e.g., >33% or >6 on follow-up imaging), persistent hemodynamic instability, or worsening neurological status, prompting consideration of more aggressive interventions.

Surgical Interventions

Surgical intervention is indicated for hematomas that are expanding, causing neurological compromise, or leading to , as these conditions can result in irreversible tissue damage or life-threatening complications. For instance, in cases of intracranial hematomas, is recommended when the hematoma thickness exceeds 10 mm or surpasses 5 mm on imaging, regardless of the patient's initial neurological status. Similarly, for epidural hematomas greater than 30 cm³, prompt evacuation is advised to prevent herniation. In peripheral or muscular hematomas, intervention is warranted if there is ongoing expansion, significant pain, or neurovascular compromise. Common surgical procedures for hematoma management include (I&D), which is particularly useful for superficial or liquefied collections, involving a small incision to evacuate the clot followed by to remove debris. For intracranial hematomas, allows direct access to evacuate the blood and control underlying vascular sources, often combined with duraplasty to prevent recurrence. In visceral hematomas, such as those in the or liver, laparoscopic repair may be employed for hemodynamically stable patients, enabling minimally invasive evacuation and through ports rather than open . serves as an alternative for hematomas arising from identifiable vascular sources, such as pseudoaneurysms, by occluding the feeding vessel endovascularly. Postoperative care following hematoma surgery typically involves the placement of drains to facilitate ongoing evacuation of residual fluid and prevent reaccumulation, with serial monitoring of output volume and character. Antibiotics are administered prophylactically or therapeutically if is suspected, and patients are closely observed for signs of rebleeding or neurological deterioration, often in an intensive care setting for intracranial cases. management includes sterile dressings and elevation to minimize swelling, with encouraged as tolerated to promote recovery. Recent advances in surgical techniques emphasize minimally invasive options to reduce morbidity, such as minimally invasive trans-sulcal parafascicular evacuation using tubular retractors, which can achieve a mean hematoma volume reduction of about 73%, with evidence of improved functional outcomes in select patients compared to medical management alone. embolization has emerged as an effective adjunct or standalone procedure for chronic subdural hematomas, achieving recurrence rates as low as 5.5% when combined with drainage, compared to 26.3% with drainage alone. Endoscopic evacuation techniques further enhance precision in select spontaneous cases, showing improved functional outcomes and reduced mortality compared to conservative management. These approaches prioritize early intervention within 8 hours to limit secondary brain injury.

Prognosis and Prevention

Prognosis

The prognosis of a hematoma varies widely depending on its size, location, timeliness of intervention, and patient comorbidities such as age and . Larger hematomas are associated with worse outcomes across types; for instance, in spontaneous spinal epidural hematomas, greater hematoma size correlates with poorer prognosis, often necessitating urgent intervention. Hematoma volume similarly serves as a key predictor in (ICH), where volumes exceeding 60 mL typically require surgical management to mitigate risks. Location further influences recovery, with ICH site (e.g., deep vs. lobar) significantly affecting functional outcomes. Timely intervention substantially improves prognosis, especially for intracranial hematomas. In severe hypertensive ICH, surgical evacuation within 6 hours of onset yields superior results, including a 40.43% rate of good functional recovery at 3 months and only 2.13% mortality, compared to 21.57% good recovery and 5.88% mortality for operations performed 6-24 hours post-onset. Delays beyond this window increase complication risks and reduce quality-of-life metrics. Comorbidities exacerbate these challenges; advanced age predicts poor outcomes, with mortality reaching 75% in patients over 50 with acute subdural hematoma, versus 25% in those aged 18-30. Coagulopathy is common in traumatic intracranial hemorrhage but does not independently increase mortality risk. Recovery timelines differ by hematoma type and severity. Superficial hematomas, such as those in soft tissues or , generally resolve spontaneously within 1-4 weeks through natural , aided by rest and compression. Chronic hematomas, however, may persist for several weeks to months, frequently resulting in residual scarring or that can impair mobility or cause cosmetic issues. Mortality remains low for peripheral hematomas overall, with traumatic muscular types showing negligible rates due to favorable spontaneous resolution, though spontaneous cases carry 4-20% mortality, particularly in anticoagulated elderly patients. Intracranial hematomas, by contrast, exhibit high mortality, reaching approximately 40% at 1 month for ICH, with untreated large lesions approaching or exceeding 50% due to compression and secondary . Recent advances, such as embolization (MMAE) for chronic subdural hematomas, have shown to reduce recurrence rates significantly when combined with , improving prognosis as of 2024-2025.

Prevention Strategies

Preventing hematomas begins with strategies to minimize trauma, a primary cause of these collections of . In vehicular contexts, consistent use of seatbelts significantly reduces the risk of blunt force injuries that can lead to hematomas, particularly in the or chest. For sports and recreational activities, wearing appropriate protective gear such as helmets during contact sports like football or decreases the incidence of head trauma, which is a common precursor to epidural or subdural hematomas. Mouthguards and padding in activities like or further mitigate facial and soft tissue impacts that might otherwise result in localized hematomas. Peri-procedural measures are essential in medical settings to avert iatrogenic hematomas. After subcutaneous injections, such as those for administration, applying firm pressure to the site for several minutes immediately post-injection helps seal puncture sites and reduces the formation of hematomas or bruising. Similarly, in procedures like , using compression devices or cold compresses for 15-20 minutes afterward can prevent hematoma development at the access site by promoting and . Effective medical management of plays a critical role in at-risk populations. For patients on , regular monitoring of the international normalized ratio (INR) to maintain levels within the therapeutic range, typically 2.0-3.0, minimizes bleeding risks including hematoma formation. In elderly individuals or those with suspected coagulopathies, preoperative screening through coagulation panels such as and identifies underlying disorders, allowing for corrective measures like factor replacement before invasive procedures. Lifestyle interventions targeting fall-prone groups, such as those with , substantially lower hematoma incidence by addressing environmental and physical risks. Implementing home modifications like installing grab bars, removing loose rugs, and ensuring adequate lighting reduces fall hazards, while balance and exercises improve stability and prevent injuries like subdural hematomas from head impacts. Assistive devices such as canes or walkers further support mobility in older adults, decreasing the likelihood of trauma-induced bleeding.

History and Etymology

Historical Context

The recognition of hematomas as localized collections of extravasated blood dates back to ancient medicine, where early descriptions appear in the around 400 BCE. In treatises such as "On Injuries of the Head," described symptoms of cranial trauma, including swellings from blood influx in wounds, emphasizing the prognostic significance of such collections in , distinguishing them from mere contusions based on clinical signs like localized swelling and neurological deficits. In the , pathological studies advanced the understanding of hematomas by integrating and cellular theory. , a pioneering pathologist, first described chronic subdural hematomas in 1857 as "pachymeningitis hemorrhagica interna," characterizing them as inflammatory lesions of the . Surgical milestones for intracranial hematomas emerged in the late , shifting from conservative observation to active intervention. In 1883, British surgeon William Henry Hulke reported the first successful evacuation of a chronic subdural hematoma via trephination, marking a pivotal advancement in neurosurgical technique. By the 1890s, procedures such as for epidural and subdural hematoma removal gained traction, though mortality remained high due to limited and infection control. The 20th century's imaging revolution, particularly the advent of computed tomography (CT) in the 1970s, fundamentally transformed diagnosis. Invented by in 1971 and first clinically applied in 1973, CT enabled rapid, non-invasive detection of hyperdense blood collections, supplanting and for intracranial cases. This led to earlier interventions, reducing diagnostic delays from days to hours and improving survival rates for conditions like epidural hematomas. Prior to the widespread availability of antibiotics in the , surgical evacuation of hematomas often resulted in fatal postoperative infections, with mortality exceeding 50% for intracranial procedures due to bacterial contamination. The penicillin era mitigated these risks, facilitating safer craniotomies and broader adoption of . From the 1980s onward, ascended as a dominant approach, introducing minimally invasive techniques like catheter drainage for extracranial and some intracranial collections, as well as for controlling underlying vascular sources of bleeding, thereby reducing operative morbidity compared to traditional open methods.

Etymology

The term "hematoma" originates from roots, combining "haîma" (αἷμα), meaning "blood," with the suffix "-ōma" (ὠμα), which denotes a swelling, mass, or tumor-like formation. This compound structure reflects classical Greek medical for pathological accumulations, where "-ōma" was commonly appended to roots describing bodily substances or conditions to indicate resultant growths or effusions. The word entered English medical literature in the mid-19th century, with the earliest documented use of the variant "haematoma" appearing around 1849–1852 in Robert Bentley's Todd's Cyclopædia of Anatomy and Physiology, a seminal compiling contemporary anatomical knowledge. Its adoption evolved from broader descriptions of blood-related pathologies, such as effusions or coagulated masses noted in Hippocratic texts, though the specific "hematoma" represents a modern synthesis rather than a direct classical term. The spelling "haematoma," prevalent in , incorporates the Latinized diphthong "ae" derived from Greek "ai," highlighting influences from medical translations that adapted Greek terminology through Latin intermediaries. Etymologically, "hematoma" is distinct from related terms like "," which combines "" (blood) with "angeîon" (ἀγγεῖον, vessel) and "-ōma" to describe a benign proliferation of vessels forming a tumor, rather than a passive collection of extravasated . This differentiation underscores how Greek roots were repurposed in 19th-century to classify vascular anomalies versus traumatic swellings.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK519551/
  2. https://www.rxlist.com/hematoma/drugs-condition.htm
  3. https://www.mayoclinic.org/diseases-conditions/intracranial-hematoma/symptoms-causes/syc-20356145
  4. https://www.medicalnewstoday.com/articles/324831
  5. https://www.mayoclinic.org/diseases-conditions/intracranial-hematoma/diagnosis-treatment/drc-20356149
  6. https://www.ncbi.nlm.nih.gov/mesh?Db=mesh&Cmd=DetailsSearch&Term=%2522Hematoma%2522%255BMeSH%2BTerms%255D
  7. https://www.cancer.gov/publications/dictionaries/cancer-terms/def/hematoma
  8. https://my.clevelandclinic.org/health/diseases/hematoma
  9. https://www.healthline.com/health/hematoma-vs-hemorrhage
  10. https://onlinelibrary.wiley.com/doi/10.1155/2017/4634350
  11. https://www.verywellhealth.com/ecchymosis-4773870
  12. https://www.emedicinehealth.com/hematoma_v_ecchymosis/article_em.htm
  13. https://www.sciencedirect.com/topics/neuroscience/hemostasis
  14. https://www.ncbi.nlm.nih.gov/books/NBK253/
  15. https://www.ncbi.nlm.nih.gov/books/NBK557613/
  16. https://www.ncbi.nlm.nih.gov/books/NBK482253/
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC5296258/
  18. https://onlinelibrary.wiley.com/doi/10.1002/term.2622
  19. https://emedicine.medscape.com/article/1137207-overview
  20. https://www.ncbi.nlm.nih.gov/books/NBK470338/
  21. https://orthoinfo.aaos.org/en/diseases--conditions/muscle-contusion-bruise/
  22. https://www.ncbi.nlm.nih.gov/books/NBK518982/
  23. https://my.clevelandclinic.org/health/diseases/22034-epidural-hematoma
  24. https://www.ncbi.nlm.nih.gov/books/NBK558928/
  25. https://pmc.ncbi.nlm.nih.gov/articles/PMC10279903/
  26. https://my.clevelandclinic.org/health/diseases/subungual-hematoma
  27. https://www.orthobullets.com/hand/6109/nail-bed-injury
  28. https://www.dynamed.com/condition/splenic-injury-and-rupture-in-adults
  29. https://pubs.rsna.org/doi/full/10.1148/radiol.2021202917
  30. https://www.ncbi.nlm.nih.gov/books/NBK525951/
  31. https://www.ncbi.nlm.nih.gov/books/NBK608612/
  32. https://pmc.ncbi.nlm.nih.gov/articles/PMC5581373/
  33. https://www.ncbi.nlm.nih.gov/books/NBK551607/
  34. https://pmc.ncbi.nlm.nih.gov/articles/PMC11259365/
  35. https://www.ncbi.nlm.nih.gov/books/NBK459222/
  36. https://pmc.ncbi.nlm.nih.gov/articles/PMC3224508/
  37. https://www.dynamed.com/condition/spontaneous-retroperitoneal-hemorrhage
  38. https://pmc.ncbi.nlm.nih.gov/articles/PMC9062138/
  39. https://pmc.ncbi.nlm.nih.gov/articles/PMC5386168/
  40. https://www.ninds.nih.gov/health-information/disorders/arteriovenous-malformations-avms
  41. https://pmc.ncbi.nlm.nih.gov/articles/PMC4688318/
  42. https://pmc.ncbi.nlm.nih.gov/articles/PMC6460605/
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC4790073/
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC4447883/
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC10366872/
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC10413390/
  47. https://pubmed.ncbi.nlm.nih.gov/32656009/
  48. https://pubmed.ncbi.nlm.nih.gov/35765987/
  49. https://pmc.ncbi.nlm.nih.gov/articles/PMC3051203/
  50. https://myhealth.alberta.ca/Health/aftercareinformation/pages/conditions.aspx?hwid=zx4360
  51. https://www.webmd.com/skin-problems-and-treatments/bruises-article
  52. https://my.clevelandclinic.org/health/diseases/15315-compartment-syndrome
  53. https://pmc.ncbi.nlm.nih.gov/articles/PMC9340208/
  54. https://pmc.ncbi.nlm.nih.gov/articles/PMC10820223/
  55. https://www.ncbi.nlm.nih.gov/books/NBK556121/
  56. https://pubmed.ncbi.nlm.nih.gov/32664886/
  57. https://my.clevelandclinic.org/health/diseases/21183-subdural-hematoma
  58. https://pmc.ncbi.nlm.nih.gov/articles/PMC10405872/
  59. https://emedicine.medscape.com/article/1137065-clinical
  60. https://www.droracle.ai/articles/347499/physical-exam-findings-of-hematoma
  61. https://www.osmosis.org/answers/neurovascular-assessment
  62. https://emedicine.medscape.com/article/1137207-clinical
  63. https://www.ncbi.nlm.nih.gov/books/NBK519033/
  64. https://emedicine.medscape.com/article/776871-workup
  65. https://theultrasoundjournal.springeropen.com/articles/10.1186/s13089-017-0060-5
  66. https://www.emdocs.net/extremity-hematoma-consider-imaging-studies-admission/
  67. https://emedicine.medscape.com/article/1137207-workup
  68. https://www.nature.com/articles/s41591-023-02620-0
  69. https://www.cancer.gov/about-cancer/causes-prevention/risk/radiation/pediatric-ct-scans
  70. https://www.aafp.org/pubs/afp/issues/2022/0600/p602.html
  71. https://www.aafp.org/pubs/afp/issues/2008/0415/p1117.html
  72. https://pmc.ncbi.nlm.nih.gov/articles/PMC5771901/
  73. https://www.ncbi.nlm.nih.gov/books/NBK532970/
  74. https://www.ncbi.nlm.nih.gov/books/NBK553103/
  75. https://emedicine.medscape.com/article/373694-overview
  76. https://www.ncbi.nlm.nih.gov/books/NBK531499/
  77. https://www.aast.org/asset/1EDF1B04-6B52-4E7B-9130ACA30413089D/
  78. https://www.ahajournals.org/doi/10.1161/01.STR.32.4.891
  79. https://pmc.ncbi.nlm.nih.gov/articles/PMC3743539/
  80. https://pmc.ncbi.nlm.nih.gov/articles/PMC6851029/
  81. https://www.ncbi.nlm.nih.gov/books/NBK470382/
  82. https://pmc.ncbi.nlm.nih.gov/articles/PMC5847253/
  83. https://radiopaedia.org/articles/aast-spleen-injury-scale?lang=us
  84. https://my.clevelandclinic.org/health/treatments/rice-method
  85. https://www.webmd.com/first-aid/rice-method-injuries
  86. https://pmc.ncbi.nlm.nih.gov/articles/PMC3501912/
  87. https://www.uptodate.com/contents/subdural-hematoma-in-adults-management-and-prognosis
  88. https://www.amboss.com/us/knowledge/epidural-hematoma/
  89. https://www.ahajournals.org/doi/10.1161/STR.0000000000000407
  90. https://emedicine.medscape.com/article/776871-medication
  91. https://www.droracle.ai/articles/145793/what-is-the-management-for-an-increasing-size-hematoma
  92. https://pmc.ncbi.nlm.nih.gov/articles/PMC8607705/
  93. https://emedicine.medscape.com/article/1916662-treatment
  94. https://pmc.ncbi.nlm.nih.gov/articles/PMC7380105/
  95. https://www.droracle.ai/articles/79984/hematoma-when-is-it-surgical-
  96. https://pubmed.ncbi.nlm.nih.gov/16710968/
  97. https://braintrauma.org/coma/guidelines/surgical
  98. https://myacare.com/blog/when-does-a-hematoma-need-to-be-drained
  99. https://fpnotebook.com/Surgery/Procedure/SbctnsHmtmDrng.htm
  100. https://emedicine.medscape.com/article/247472-overview
  101. https://pmc.ncbi.nlm.nih.gov/articles/PMC4613419/
  102. https://pmc.ncbi.nlm.nih.gov/articles/PMC11079242/
  103. https://my.clevelandclinic.org/health/drugs/15199-surgical-drains
  104. https://neurospinesurgical.com/wp-content/uploads/2017/09/surgery-subdural-hematoma.pdf
  105. https://www.nejm.org/doi/full/10.1056/NEJMoa2308440
  106. https://snisonline.org/new-research-shows-minimally-invasive-therapy-middle-meningeal-artery-embolization-is-effective-in-treating-chronic-subdural-hematoma/
  107. https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(24)00578-9/fulltext
  108. https://www.ahajournals.org/doi/10.1161/STROKEAHA.124.047467
  109. https://iv.iiarjournals.org/content/invivo/38/5/2415.full.pdf
  110. https://pmc.ncbi.nlm.nih.gov/articles/PMC11839887/
  111. https://www.nature.com/articles/s41598-024-81106-6
  112. https://pmc.ncbi.nlm.nih.gov/articles/PMC8430150/
  113. https://pubmed.ncbi.nlm.nih.gov/8512021/
  114. https://link.springer.com/article/10.1007/s00701-021-04808-0
  115. https://www.medicinenet.com/how_long_does_it_take_for_a_hematoma_to_go_away/article.htm
  116. https://larkinhealth.com/en/treatments-services/vascular/hematoma/
  117. https://pmc.ncbi.nlm.nih.gov/articles/PMC5881146/
  118. https://www.ahajournals.org/doi/10.1161/STROKEAHA.120.032550
  119. https://www.buffalo.edu/ubnow/stories/2024/11/davies-nejm-subdural-hematoma.html
  120. https://www.ahajournals.org/doi/10.1161/SVIN.125.001814
  121. https://pmc.ncbi.nlm.nih.gov/articles/PMC2987604/
  122. https://pmc.ncbi.nlm.nih.gov/articles/PMC7841679/
  123. https://pmc.ncbi.nlm.nih.gov/articles/PMC6485505/
  124. https://pubmed.ncbi.nlm.nih.gov/39822338/
  125. https://pmc.ncbi.nlm.nih.gov/articles/PMC6838915/
  126. https://pmc.ncbi.nlm.nih.gov/articles/PMC3760283/
  127. https://www.ncbi.nlm.nih.gov/books/NBK606118/
  128. https://pmc.ncbi.nlm.nih.gov/articles/PMC8791143/
  129. https://www.ncbi.nlm.nih.gov/books/NBK560761/
  130. https://www.ncbi.nlm.nih.gov/books/NBK553101/
  131. https://pmc.ncbi.nlm.nih.gov/articles/PMC7093636/
  132. https://classics.mit.edu/Hippocrates/headinjur.13.13.html
  133. https://pubmed.ncbi.nlm.nih.gov/15040710/
  134. https://pmc.ncbi.nlm.nih.gov/articles/PMC6517544/
  135. https://jamanetwork.com/journals/jama/fullarticle/398093
  136. https://pmc.ncbi.nlm.nih.gov/articles/PMC6992895/
  137. https://pmc.ncbi.nlm.nih.gov/articles/PMC3036249/
  138. https://www.sciencedirect.com/science/article/pii/S1878788613000702
  139. https://www.etymonline.com/word/hematoma
  140. https://radiopaedia.org/articles/hematoma-1?lang=us
  141. https://www.etymonline.com/word/-oma
  142. https://www.oed.com/dictionary/haematoma_n
  143. https://pmc.ncbi.nlm.nih.gov/articles/PMC3065807/
  144. https://www.etymonline.com/word/hemato-
  145. https://www.clinicalanatomy.com/mtd/745-hemangioma-hemangiomata
  146. https://www.oed.com/dictionary/haemangioma_n
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