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Nosebleed

A nosebleed, medically termed epistaxis, is the hemorrhage from the blood vessels of the , most commonly originating from the highly vascular anterior known as . These bleeds are typically anterior (90% of cases) and self-limiting, but posterior epistaxis, arising from larger vessels in the posterior , can be more severe and life-threatening. Epistaxis affects about 60% of people during their lifetime, with only around 10% requiring medical attention, and is most prevalent in children aged 2-10 and adults over 50. The condition arises from a rupture of superficial nasal blood vessels, often due to local such as , dry air, or upper respiratory infections, which irritate and weaken the fragile nasal lining containing numerous delicate capillaries close to the surface. Systemic factors like , medications (e.g., or aspirin), bleeding disorders (e.g., hemophilia or ), and environmental irritants such as chemical exposure or use can exacerbate or trigger episodes. Less common etiologies include nasal tumors, polyps, or hereditary conditions like , while allergies, deviated septum, and overuse of nasal decongestants contribute to recurrent cases. Symptoms usually involve unilateral bleeding from one , though bilateral flow can occur if blood drains posteriorly into the , potentially causing of blood, , or difficulty in severe instances. Most episodes are minor and resolve spontaneously or with simple first-aid measures, such as pinching the nostrils for 10-15 minutes while leaning forward to allow the blood to drain out and prevent it from flowing down the . Management escalates based on severity: topical vasoconstrictors like , chemical or electrical cautery for visible vessels, or nasal packing for persistent bleeding; posterior bleeds may necessitate hospitalization, , or surgical . Prevention strategies include humidifying indoor air, applying to nasal passages, avoiding nasal irritants, and managing underlying conditions like or coagulopathies. Individuals should seek immediate medical care for nosebleeds lasting over 20-30 minutes, recurring frequently, occurring after , or in those on blood thinners, as these may signal complications like significant blood loss or underlying .

Signs and symptoms

Presentation

A nosebleed, or epistaxis, typically presents with a sudden onset of from one or both nostrils, often manifesting as due to its arterial origin in the anterior . In most cases, the bleeding is unilateral and visible externally, though posterior bleeds may primarily drain into the nasopharynx, leading to appearing in the or . Associated symptoms include , where flows backward into the , potentially causing a metallic or bad taste in the from swallowed . Severe episodes may involve difficulty or if accumulates in the airway, along with mild irritation or discomfort at the bleeding site. The volume and duration of bleeding range from minor spotting that resolves in seconds to profuse hemorrhage lasting minutes to hours, with anterior bleeds generally milder and posterior ones more voluminous. Patients should seek emergency care for heavy bleeding that soaks through tissues within minutes, persists beyond 20 minutes despite pressure, or causes , , or respiratory distress from .

Classification

Nosebleeds, or epistaxis, are primarily classified by their anatomical location within the , with anterior epistaxis accounting for approximately 90% of cases and originating from the on the anterior . This type is typically unilateral, presents with steady bleeding that is visible in the anterior nares, and is easier to control through simple measures such as pinching the nostrils or local cautery. In contrast, posterior epistaxis comprises about 10% of cases and arises from the in the posterior , often involving branches of the . Posterior bleeds are generally more severe, frequently bilateral due to blood draining forward from the back of the nose, and harder to manage, often requiring hospitalization and advanced interventions like nasal packing or . The severity of epistaxis varies, with most cases being minor and self-limited, while severe cases may involve significant blood loss leading to hemodynamic , hospitalization, and potentially requiring transfusion. This helps guide urgency of care, as severe epistaxis can lead to complications like or airway compromise, particularly in vulnerable populations such as the elderly or those with comorbidities. Epistaxis can also be categorized by recurrence patterns, distinguishing primary epistaxis as idiopathic and recurrent without an identifiable underlying cause, often frequent and self-perpetuating due to local vascular fragility, from secondary epistaxis, which is linked to specific etiologies such as , medications, or systemic diseases and may present as single or recurrent episodes depending on the trigger. This differentiation is crucial for diagnostic , as recurrent primary cases may warrant preventive measures, while secondary cases require addressing the root cause. Special types of epistaxis include those associated with (HHT), a characterized by abnormal formation leading to recurrent, often severe nosebleeds in over 90% of affected individuals due to telangiectasias in the . Iatrogenic epistaxis, another distinct category, occurs as a complication following nasal or sinus procedures, such as or , resulting from vascular injury or formation. These subtypes highlight the need for tailored management strategies beyond standard classifications.

Causes and risk factors

Local causes

Local causes of nosebleed, or epistaxis, primarily involve direct insults to the and underlying vasculature, often leading to rupture of superficial vessels in or other anterior nasal sites. These factors are distinct from systemic conditions and typically result in anterior epistaxis, which accounts for the majority of cases. Common local triggers include mechanical , environmental irritants, structural nasal abnormalities, , iatrogenic interventions, and certain habitual behaviors. Trauma represents one of the most frequent local precipitants of epistaxis, encompassing both intentional and accidental injuries to the nasal lining. , also known as epistaxis digitorum, causes mucosal ulceration and vessel damage through repeated digital manipulation, particularly in children and young adults. Facial injuries from blows, falls, or sports can fracture or lacerate mucosa, resulting in immediate or delayed . In pediatric populations, foreign bodies such as toys or food particles inserted into the may erode the mucosa over time, provoking and hemorrhage. Environmental factors contribute by compromising the integrity of the , often through or . Low , prevalent in arid climates, heated indoor environments, or during winter months, dries the nasal lining, leading to crusting, cracking, and subsequent vessel exposure and rupture. Allergens and irritants, including , chemical fumes, or pollutants, can inflame the mucosa in susceptible individuals, exacerbating dryness and fragility. Structural and pathological nasal conditions predispose individuals to recurrent epistaxis by altering , promoting irritation, or directly invading vessels. Septal deviations or spurs disrupt normal nasal , causing localized dryness and mucosal on the affected side. Nasal polyps, which are benign growths arising from inflammation, can obstruct passages and lead to upon or . Tumors, whether benign (e.g., angiofibromas) or malignant (e.g., squamous carcinomas), may cause epistaxis through vascular or , often presenting with unilateral symptoms. Infections such as acute or and (bacterial, viral, or allergic) inflame the mucosa, increasing vascular and risk, particularly during episodes of sneezing or forceful . Iatrogenic causes arise from medical procedures or therapies that inadvertently damage nasal structures. Postoperative bleeding following or other nasal surgeries occurs due to mucosal lacerations or vessel transection, with risks heightened in the immediate recovery period. Nasotracheal , often used in or critical care, can traumatize the and mucosa through mechanical friction. Overuse of topical nasal sprays, including decongestants or corticosteroids, may cause rebound congestion, mucosal atrophy, or irritation, predisposing to epistaxis. Certain habitual behaviors directly erode nasal tissues, leading to chronic or severe epistaxis. Intranasal use, common in adolescents and adults, causes followed by mucosal ischemia, ulceration, and septal , resulting in persistent sites.

Systemic causes

Systemic causes of nosebleed, or epistaxis, encompass conditions and factors that affect , vascular integrity, or overall across the body, increasing susceptibility to episodes from nasal vessels. These differ from local nasal factors by involving multifocal physiological disruptions, such as impaired clotting mechanisms or elevated vascular pressures that can precipitate or exacerbate epistaxis. Coagulation disorders represent a primary category of systemic contributors to epistaxis. Hemophilia A and B, hereditary deficiencies in and IX respectively, lead to prolonged after minor trauma, with epistaxis being a frequent manifestation due to deficient clot formation. , the most common inherited disorder, impairs platelet adhesion and stabilizes , often presenting with recurrent epistaxis alongside mucosal . , characterized by low platelet counts, disrupts primary and heightens epistaxis risk, particularly when counts fall below 50,000/μL, as platelets are essential for initial vessel constriction and plug formation. Vascular diseases further predispose individuals to epistaxis through altered blood flow dynamics or structural weaknesses. elevates intranasal vascular pressure, straining fragile anterior septal vessels and accounting for a significant portion of adult epistaxis cases, though its role may be more associative than directly causative in all instances. (HHT), an autosomal dominant disorder, causes abnormal arteriovenous malformations and telangiectasias, with recurrent epistaxis emerging as the hallmark symptom in nearly all affected individuals by age 40 due to fragile vessels. Medications that interfere with substantially elevate epistaxis risk. Anticoagulants such as inhibit vitamin K-dependent clotting factors, prolonging bleeding time and increasing epistaxis incidence, particularly when combined with other risk factors. Antiplatelet agents like aspirin and clopidogrel, along with nonsteroidal drugs (NSAIDs), impair platelet aggregation, leading to higher rates of mucosal bleeding including epistaxis; for instance, aspirin use is linked to a twofold increase in severe cases requiring intervention. Systemic illnesses compromising pathways also contribute. Liver disease reduces synthesis of clotting factors II, VII, IX, and X, alongside from splenic sequestration, resulting in epistaxis as part of a broader . Renal failure induces , which causes platelet dysfunction through accumulation and , predisposing to epistaxis via impaired primary . , often secondary to or use, depletes factors II, VII, IX, and X, manifesting as epistaxis in both adults and neonates due to resultant . Additional factors include physiological states and habits affecting . Pregnancy increases blood volume by 40-50% and elevates levels, promoting vascularity and congestion, which heightens epistaxis frequency, especially in the third . Alcohol abuse impairs liver function, leading to and , while acute may vasodilate nasal vessels, both contributing to recurrent epistaxis.

Pathophysiology

Vascular anatomy

The nasal vasculature derives its arterial supply from branches of both the internal and external carotid arteries, creating a rich network that supports the organ's functions but also predisposes it to bleeding. The internal carotid contributes via the , which gives rise to the anterior and posterior ethmoidal arteries; these supply the superior and lateral walls. The external carotid provides the majority of flow through its branches—the (supplying the posterior and lateral walls), (anterior and floor), and (posterior wall)—as well as the superior labial artery from the (anterior and ). Anterior bleeding typically arises from , also known as Little's area, an anastomotic network on the anteroinferior formed by the convergence of the anterior ethmoidal, sphenopalatine, greater palatine, and superior labial arteries. This region accounts for approximately 90% of epistaxis cases and exemplifies the watershed-like vulnerability where terminal branches meet. Posterior bleeding often originates from the area traditionally known as , located along the posterior lateral nasal wall near the inferior turbinate; while commonly described as comprising branches of the sphenopalatine and ascending pharyngeal arteries, recent anatomical studies suggest it may be primarily a venous plexus. Venous drainage parallels the arterial supply, with interconnecting pathways that include the facial vein for anterior structures, the for lateral walls via maxillary veins, and ophthalmic veins for superior ethmoidal regions; these ultimately converge into the . The valveless nature of these veins and their connections to extracranial and intracranial plexuses, such as the , render the system susceptible to pressure fluctuations that can exacerbate bleeding. The consists of a thin, pseudostratified ciliated columnar overlying a vascular , where capillaries and small vessels lie in close proximity to , facilitating air humidification but increasing susceptibility to and rupture. Extensive anastomoses between internal and external carotid-derived arteries, particularly within Kiesselbach's and Woodruff's plexuses, form a highly interconnected network that amplifies bleeding potential by allowing retrograde flow and recruitment of collateral vessels during hemorrhage. In older adults, age-related vascular changes such as lead to wall thickening, fragility, and reduced elasticity, particularly in the , heightening epistaxis risk through impaired and easier rupture.

Bleeding mechanisms

Nosebleeds, or epistaxis, often initiate through fragility in the , particularly where the is thin and susceptible to damage. Endothelial damage from , such as digital manipulation or forceful , or from environmental dryness leading to mucosal cracking, exposes the subendothelium and triggers rupture. This fragility is especially pronounced in areas like , where superficial vessels are prone to minor insults. Dryness exacerbates this by reducing mucosal hydration, causing epithelial erosion and subsequent bleeding. Hemodynamic factors contribute significantly to the onset and persistence of bleeding by imposing mechanical stress on vulnerable vessels. Elevated increases hydrostatic pressure within nasal capillaries, promoting vessel wall distension and potential rupture, while also prolonging hemorrhage duration through sustained flow. In hypertensive individuals, this can lead to higher on endothelial surfaces, further weakening vessel integrity and facilitating epistaxis. Coagulation failure impairs the hemostatic response, allowing initial bleeds to escalate. Deficiencies in platelet adhesion, often due to medications like aspirin or conditions such as , hinder the formation of stable platelet plugs at the injury site. Similarly, disruptions in formation from anticoagulants like or inherited coagulopathies such as hemophilia prolong bleeding by preventing effective clot stabilization. Inflammatory responses in the can precipitate or worsen epistaxis through localized vascular changes. Infections or allergic conditions, such as , induce and increased via mediators like , which erode mucosal barriers and expose vessels to rupture. This heightened permeability allows plasma extravasation, further irritating tissues and promoting bleeding episodes. Recurrent epistaxis can establish vicious cycles that progressively weaken local tissues. Repeated minor bleeds cause cumulative endothelial injury and fibrosis, reducing vascular resilience and increasing susceptibility to future hemorrhages, particularly in conditions like . Over time, this chronic trauma fosters a of inflammation and tissue remodeling that sustains the risk of recurrent bleeding.

Diagnosis

Clinical assessment

Clinical assessment of nosebleed, or epistaxis, begins with a thorough to characterize the episode and identify potential underlying factors. Healthcare providers inquire about the onset (sudden or gradual), duration, frequency of episodes, and laterality (unilateral or bilateral), as well as any inciting events such as , recent nasal manipulation, or environmental exposures. Associated symptoms are evaluated, including , facial pain, , or , which may indicate significant blood loss or other complications; a of easy bruising, prolonged bleeding from other sites, or family history of bleeding disorders is also elicited to screen for coagulopathy. Medication use, particularly anticoagulants, antiplatelet agents, or nonsteroidal anti-inflammatory drugs, is documented, along with comorbidities like hypertension or liver disease that could contribute to bleeding risk. The starts with assessment of to evaluate hemodynamic stability, as or may signal substantial blood loss from ongoing or recurrent epistaxis. Mental status and airway patency are checked to rule out immediate threats, particularly in cases of profuse bleeding. Nasal inspection follows, ideally with the patient seated upright and forward-leaning to minimize posterior drainage; a bright light source, nasal speculum, and suction are used to clear clots and visualize the , focusing on the anterior and where most bleeds originate. Anterior rhinoscopy, performed with a nasal speculum and headlight, allows direct visualization of the bleeding site in approximately 90% of cases, which are anterior in location and often amenable to targeted . Topical vasoconstrictors like epinephrine may be applied to facilitate by reducing , though is taken to avoid overuse in patients with cardiovascular risks. If bleeding persists despite initial compression, the exam helps differentiate anterior from posterior sources: anterior bleeds typically present as visible from one , while posterior bleeds are characterized by occult drainage into the , bilateral involvement, or high-volume output that is harder to localize. Red flags during assessment prompt urgent further evaluation, including signs of anemia such as or from chronic or heavy blood loss, a personal history of , or symptoms suggestive of neoplasms like unilateral nasal obstruction or recurrent unilateral bleeding. Airway compromise, hemorrhagic shock, or unrelenting profuse bleeding also warrant immediate stabilization and specialist referral.

Diagnostic tests

When initial clinical assessment fails to identify the source or cause of epistaxis, laboratory tests are employed to evaluate for underlying hematologic abnormalities or the need for transfusion support. A (CBC) is recommended to assess for due to blood loss, , or suggestive of or . studies, including (PT), (PTT), and international normalized ratio (INR), are indicated if a bleeding diathesis is suspected, such as in patients on anticoagulants or with . For severe or ongoing bleeding, blood typing and cross-matching (type/screen) prepare for potential transfusion. Imaging modalities are reserved for cases where structural lesions or vascular anomalies are suspected, particularly in recurrent or unilateral epistaxis. Computed tomography (CT) scans of the and can detect tumors, vascular malformations, or erosive lesions causing hemorrhage, while (MRI) provides superior soft tissue detail for neoplasms or extensions into adjacent structures. Nasal , using flexible or rigid scopes, is a key diagnostic tool for visualizing posterior bleeding sites not accessible by speculum examination alone, allowing direct identification and potential intervention. In severe recurrent cases refractory to initial management, identifies vascular sources such as pseudoaneurysms or arteriovenous malformations, guiding procedures. If is suspected based on unilateral or persistent symptoms, of suspicious lesions confirms , while testing may be considered in atopic patients with inflammatory contributing to fragility. For hospitalized patients with significant blood loss, serial monitoring of levels tracks hemodynamic stability and transfusion requirements.

Prevention

General measures

Maintaining nasal is a foundational strategy for preventing nosebleeds, particularly in at-risk populations such as the elderly, who experience higher incidence due to factors like reduced clotting efficiency and comorbidities. Using a in indoor spaces, especially during dry seasons, adds to the air and helps preserve the integrity of nasal mucous membranes. Similarly, regular application of saline nasal sprays or drops, 2-3 times daily, keeps nasal passages hydrated without causing irritation. Avoiding environmental and behavioral irritants further reduces the risk of mucosal fragility leading to bleeding. Quitting is essential, as dries and inflames nasal tissues, exacerbating vulnerability to epistaxis. Limiting consumption helps prevent and blood thinning effects that can promote nosebleeds. Protecting the nose from dry or cold air—such as by wearing a in winter or avoiding prolonged exposure to heated indoor environments—maintains mucosal . Proper nasal hygiene practices support long-term prevention by minimizing trauma to delicate blood vessels. Gentle cleaning with saline solutions avoids harsh disruption, while refraining from forceful or picking prevents vessel rupture; trimming fingernails can aid in discouraging habitual picking, especially in children. Dietary habits contribute to vascular resilience against . Adequate hydration through consistent intake of water or fluids keeps overall body moisture levels sufficient to support nasal lining integrity. Consuming foods rich in , such as citrus fruits and vegetables, promotes synthesis essential for strengthening walls, thereby reducing bleeding tendencies. For seasonal management, applying a thin layer of inside the nostrils with a , up to three times daily, acts as a barrier against dryness, particularly effective during winter when low humidity prevails.

Targeted interventions

For individuals with recurrent anterior nosebleeds, prophylactic targets the specific bleeding site to prevent future episodes. Chemical using is a outpatient that seals fragile vessels in , reducing recurrence rates in suitable cases. Electrical cautery offers a precise alternative, particularly when chemical methods are insufficient, and both approaches are effective for localized anterior epistaxis without underlying structural defects. These interventions are typically reserved for patients experiencing frequent bleeds despite general measures like humidification. Medications play a role in preventing nosebleeds among those with predisposing factors, such as coagulopathies or vascular fragility. , such as , are particularly beneficial for patients with conditions like or excessive , where they stabilize clots and reduce recurrent bleeding episodes by inhibiting plasminogen activation. Addressing underlying comorbidities is essential for targeted prevention in high-risk groups. Effective control through antihypertensive therapy lowers the risk and severity of epistaxis in patients, as uncontrolled exacerbates vessel rupture. Correcting coagulopathies, such as , involves supplementation to normalize clotting factors and prevent spontaneous bleeds; for instance, intravenous or oral rapidly restores in deficient states. Structural interventions and supportive devices target anatomical issues contributing to recurrent nosebleeds. Septal surgery, such as , corrects deviated septa that promote turbulent airflow and mucosal drying, thereby reducing epistaxis frequency in affected individuals. Nasal tampons or absorbent devices may be used for on-field management of epistaxis in sports settings, particularly for anterior bleeds from injuries. Vaccinations against respiratory infections help prevent secondary causes of nosebleeds. Annual vaccination reduces the incidence of flu-related , which can inflame and trigger epistaxis, particularly in vulnerable populations.

Treatment

Initial management

The initial management of a nosebleed, also known as epistaxis, focuses on simple, non-invasive first-aid measures to control bleeding and prevent complications such as or excessive blood loss. The patient should be positioned sitting upright with the head tilted slightly forward to minimize blood flow into the and reduce the risk of or airway obstruction. This forward lean helps drain blood out of the nostrils rather than allowing it to pool posteriorly. Direct pressure is the cornerstone of initial control, achieved by using the thumb and to pinch the soft, lower portion of the (the nostrils) firmly against the for 10 to 15 minutes without interruption. Releasing pressure prematurely to check for cessation can prolong bleeding, so continuous application is essential. Adjunctive cooling with an applied to the bridge of the can promote and aid in . Patients should avoid tilting the head backward, as this directs toward the and increases risk, and refrain from to prevent gastric irritation. Additionally, during an active bleed, aspirin or nonsteroidal drugs should not be taken, as they can exacerbate bleeding. If bleeding persists beyond 20 minutes despite these measures, involves significant blood volume (e.g., more than a ), or recurs frequently, immediate medical evaluation is necessary to rule out underlying causes or require advanced interventions. In cases of recurrent epistaxis or those occurring in patients on anticoagulants, even brief episodes warrant prompt professional assessment.

Cauterization and packing

Cauterization and packing represent key interventions for managing moderate epistaxis when initial measures fail, targeting the of visible bleeding vessels or of the to achieve . These procedures are typically performed by healthcare professionals after identifying the bleeding site, often in the anterior via clinical assessment. They are indicated for persistent bleeding not controlled by pressure or topical agents, aiming to minimize blood loss while avoiding more invasive options. Chemical involves applying agents directly to the visible bleeding point to induce localized and sealing. , commonly in a 75% , is applied via a stick or for 30 to 60 seconds, promoting protein and formation effective for anterior septal bleeds. serves as an alternative, particularly when is unavailable, by denaturing proteins and achieving similar hemostatic effects with application limited to under 10 seconds to prevent excessive damage. Both methods carry risks of septal if overused, but they offer outpatient feasibility with high success rates in uncomplicated cases. Electrical and thermal cauterization provide precise alternatives for deeper or recurrent sites, using energy to coagulate vessels without widespread chemical spread. delivers controlled heat via low-energy waves, minimizing surrounding injury and suitable for outpatient settings. therapy, such as Nd:YAG or argon lasers, targets telangiectasias or arterioles with photocoagulation, showing superior long-term efficacy in reducing rebleeding compared to some chemical methods, though it requires specialized equipment. These techniques enhance precision under endoscopic guidance, reducing complications like crusting or . Anterior packing is employed when alone is insufficient, involving insertion of absorbent materials to apply direct pressure and absorb blood. Materials such as Merocel, a compressed sponge, or layered petroleum are placed bilaterally in the nasal vestibule and , often impregnated with vasoconstrictors like or epinephrine to enhance vessel constriction and . This method controls 90% of anterior bleeds but can cause discomfort, mucosal ischemia, or infection if prolonged. For posterior epistaxis, originating from the nasopharynx or , posterior packing uses balloon catheters to isolate and compress the bleeding area. Devices like Foley catheters or dual-balloon systems (e.g., Epistat) are advanced nasally, with the posterior balloon inflated in the nasopharynx and anterior packing added for support, necessitating hospital monitoring for oxygenation and pressure adjustments. This approach halts severe posterior bleeds but risks complications such as or if mismanaged. Nasal packing, whether anterior or posterior, is generally left in place for 24 to 72 hours to allow clot stabilization, with removal timed to balance against risks like pressure or . Premature removal before 48 hours increases rebleeding likelihood, while extended duration beyond 72 hours heightens infection potential, guiding clinical decisions based on bleed severity.

Surgical and advanced therapies

Surgical and advanced therapies are indicated for severe, recurrent, or posterior epistaxis that fails to respond to initial management, such as nasal packing. These procedures are typically performed in an operating room setting and target underlying vascular or structural causes to prevent further hemorrhage. Endoscopic sphenopalatine artery ligation (ESPAL) involves tying off the , a primary blood supply to the posterior , using an for direct visualization and minimally invasive access through the . This procedure is particularly effective for posterior epistaxis, achieving hemorrhage control in approximately 90-98% of cases, with low recurrence rates when performed by experienced surgeons. Arterial embolization is a radiological that blocks feeding vessels to the , such as branches of the internal maxillary or sphenopalatine arteries, using catheter-delivered embolic materials like particles. It is reserved for patients with high anesthetic risk, failed surgical , or intractable , offering success rates of 87-93% and serving as an to open surgery. Septoplasty addresses recurrent epistaxis by surgically correcting a deviated that contributes to mucosal , dryness, or vascular fragility leading to bleeds. This reshapes the to improve and reduce , and is indicated when structural is identified as a contributing factor in persistent cases unresponsive to conservative measures. For patients with (HHT), laser therapy targets intranasal telangiectasias—dilated, fragile vessels prone to rupture—using modalities such as , Nd:YAG, , or (KTP) lasers to photocoagulate lesions and reduce bleeding frequency and severity. These treatments achieve symptom improvement in 70-90% of HHT patients, with blue light and lasers noted for minimal surrounding tissue damage compared to traditional .

Pharmacological options

Pharmacological options play an adjunctive role in managing epistaxis, particularly when initial mechanical measures are insufficient, by promoting , enhancing clot stability, reversing anticoagulation effects, preventing secondary infections, or alleviating associated pain. These interventions are typically employed in clinical settings for active or recurrent bleeding, with selections guided by the bleed's severity, underlying causes, and patient comorbidities. Guidelines emphasize their use alongside or packing rather than as standalone treatments, prioritizing agents with rapid onset and minimal systemic absorption to avoid complications like or . Topical vasoconstrictors, such as epinephrine, are commonly applied via soaked pledgets or sprays to induce local vessel contraction and facilitate in anterior epistaxis. A concentration of 1:1000 epinephrine combined with lidocaine is effective for initial control, achieving bleeding cessation in a significant proportion of cases within minutes, though care must be taken to avoid overuse due to potential cardiovascular effects in susceptible patients. Similarly, topical (TXA), an agent, is sprayed or applied directly to the bleeding site to inhibit and stabilize clots; randomized trials demonstrate it reduces rebleeding rates at 24 hours and one week compared to or standard packing, with a favorable safety profile for short-term use. For more severe or refractory epistaxis, systemic like intravenous are administered to systemically inhibit plasminogen activation, thereby preventing premature clot breakdown. A single 1-gram dose has shown efficacy in reducing postoperative nasal bleeding following procedures and in emergency settings for persistent epistaxis, particularly in patients with hyperfibrinolysis or , though evidence is stronger for topical over systemic routes in non-surgical cases. In patients on anticoagulants experiencing significant epistaxis, reversal agents are considered if bleeding is life-threatening or uncontrolled, balancing thrombotic risks. rapidly neutralizes unfractionated , while or addresses warfarin-induced by restoring vitamin K-dependent factors; for direct oral anticoagulants, specific antidotes like for or for factor Xa inhibitors are preferred when available, as per consensus pathways. Routine reversal is not recommended for mild bleeds, as continuing anticoagulation often suffices with local measures. Antibiotics are not routinely indicated for anterior nasal packing in uncomplicated epistaxis, as prophylactic systemic use does not significantly reduce rates and may promote ; however, they are prescribed if the bleed is -related (e.g., due to ) or for posterior packing, where topical options like ointment can mitigate risk. For HHT-associated epistaxis, , an oral analog, has demonstrated significant reduction in bleeding severity in clinical trials as of 2024. Pain management during or after epistaxis episodes favors acetaminophen, which provides analgesia without impairing platelet function or increasing bleeding risk, at doses up to 4 grams daily in adults. Nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin and ibuprofen, are contraindicated due to their antiplatelet effects, which can exacerbate hemorrhage.

Complications

Immediate risks

Severe epistaxis can result in substantial hemorrhage, potentially leading to if blood loss exceeds significant volumes, such as more than 20% of total , manifesting as , , and organ hypoperfusion. This risk is heightened in vulnerable populations like the elderly or those with comorbidities, though it remains rare in most cases. Aspiration of into the lungs represents another acute hazard, particularly during posterior bleeds where blood drains posteriorly into the , potentially causing if inhaled. This complication arises from the forceful flow of or dislodged clots, exacerbating respiratory distress and requiring prompt . Acute may develop rapidly from ongoing loss, resulting in a sudden drop in levels that induces symptoms such as , , , and . In severe instances, this can necessitate transfusion if falls critically low, underscoring the need for immediate hematologic evaluation. Infection risks emerge from nasal manipulation during treatment, such as packing or , which can introduce bacteria leading to , , or rarely , often mitigated by prophylactic antibiotics. Swallowed blood from epistaxis may cause gastrointestinal irritation, leading to or . Posterior epistaxis poses a particular threat of airway compromise, as profuse bleeding into the nasopharynx can obstruct breathing, potentially requiring to secure the airway and prevent asphyxiation. This obstruction risk is amplified if packing migrates or if the patient is unable to clear accumulating blood effectively.

Chronic effects

Frequent or recurrent nosebleeds, often stemming from underlying vascular fragility or environmental factors, can lead to through cumulative blood loss, manifesting as , , and . In conditions like (HHT), where epistaxis is a hallmark symptom, up to 50% of patients develop due to repeated hemorrhages, necessitating iron supplementation or transfusions to restore levels. Persistent epistaxis contributes to nasal mucosal damage, including chronic crusting and dryness that perpetuates a cycle of and . Over time, this can result in septal , particularly if complicated by repeated or self-induced from crust removal, leading to symptoms such as nasal pain, whistling sounds, and increased risk. Additionally, recurrent may exacerbate sinus issues, including chronic rhinosinusitis, by promoting inflammation and obstruction in the . In individuals with recurrent nosebleeds, psychological effects such as anxiety, social phobia, and are common, particularly in chronic conditions like HHT, where unpredictable bleeding episodes foster isolation and emotional distress. These impacts arise from the fear of sudden hemorrhages in social settings, contributing to avoidance behaviors and reduced overall well-being. Recurrent epistaxis is a frequent in cases of uncontrolled , which can heighten bleeding severity and risk of complications like significant blood loss if unmanaged. Nighttime nosebleeds further impair by disrupting sleep through sudden awakenings and anxiety, leading to daytime fatigue and diminished daily functioning.

Epidemiology

Incidence and prevalence

Nosebleeds, or epistaxis, are a common occurrence, with an estimated lifetime of 60% in the general population, meaning most individuals experience at least one episode during their lives. Of those affected, estimates vary, with approximately 6-10% seeking medical attention, highlighting that while frequent, severe cases requiring intervention are relatively uncommon. The annual incidence of epistaxis leading to emergency department visits is approximately 1.7 per 1,000 population , reflecting a stable overall rate over recent decades. Incidence exhibits a bimodal age distribution, with peaks among children aged 2 to 10 years and adults over 50 years, particularly those 70 to 79 years old, where rates can reach 12 per 1,000 visits. Seasonally, episodes are more frequent during winter months, attributed to low and dry air that irritate . Globally, prevalence varies by climate, with higher rates observed in arid regions such as the , where low humidity exacerbates nasal dryness and vessel fragility. Overall trends in epistaxis incidence remain stable as of 2025, though visits for anticoagulant-related bleeding increased during 2016-2020 due to rising use of direct oral anticoagulants.

Demographic patterns

Nosebleeds, or epistaxis, display a bimodal distribution, with notable peaks in pediatric and geriatric populations. In children, particularly those aged 2 to 10 years, epistaxis is prevalent, affecting up to 30% of children under 5 years and over 50% by 10, often stemming from trauma-related causes such as or minor nasal injuries; these cases account for approximately 1 in 200 pediatric visits. In older adults, incidence rises sharply between 60 and 80 years, driven by age-related vascular fragility, where and blood vessels become thinner and more susceptible to rupture due to natural degenerative changes. A slight male predominance exists in nosebleed occurrence, with comprising about 60-70% of cases across studies, yielding a of roughly 1.5:1 to 2:1; this disparity may relate to greater male involvement in outdoor activities and resultant nasal . Ethnic variations influence nosebleed rates, with higher incidence observed among Caucasians compared to African-Americans, potentially linked to differences in mucosal dryness and environmental factors like . Rates tend to be lower in humid regions, where drier air—a key irritant leading to vessel cracking—is less prevalent. (HHT), a genetic cause of recurrent epistaxis, affects all ethnic groups equally overall, though specific mutations show higher prevalence in certain European lineages. Socioeconomic factors may contribute to treatment disparities in epistaxis , with studies indicating variations in and interventions based on levels. Urban-rural differences also emerge, with urban dwellers facing elevated rates possibly due to and denser allergen loads, though some analyses find no significant overall gap. Comorbidities amplify nosebleed susceptibility, with hypertensive individuals experiencing about 47% higher risk of episodes requiring hospital care, owing to chronic vascular strain. users face similarly elevated risks, with studies indicating up to 50% or greater increase in bleeding events compared to non-users, due to impaired clotting mechanisms.

History and etymology

Historical context

The management of nosebleeds, or epistaxis, has evolved significantly from rudimentary ancient practices to sophisticated modern interventions, reflecting advancements in anatomical understanding and medical technology. In around 1600 BCE, treatments documented in medical papyri such as the included the use of linen plugs to tamponade bleeding sites in nasal and applications to promote clotting, marking early recognition of the need for direct pressure and hemostatic agents in nasal hemorrhage. These methods emphasized physical over systemic explanations, prioritizing immediate cessation of blood loss in an era without refined surgical tools. By the classical Greek period, (c. 460–370 BCE) advanced these approaches through systematic observation, describing with hot irons to seal bleeding vessels in the , as detailed in the . This technique, applied via specialized probes to avoid damaging surrounding tissues, represented a shift toward thermal hemostasis and is credited with being among the first instrument-based interventions for epistaxis. In the medieval era, influenced by Galenic humoral theory, nosebleeds were often interpreted as signs of excess blood or phlegm imbalance, leading to practices—such as venesection or cupping—to restore equilibrium, though this sometimes exacerbated bleeding rather than resolving it. The brought anatomical precision to epistaxis management, with the identification of the anterior nasal plexus—later termed —by Wilhelm Kiesselbach in the 1880s, highlighting the septal region's vascular vulnerability as the source of most bleeds. Concurrently, the introduction of as a in by Carl Koller revolutionized nasal procedures, enabling painless and packing without the risks of general , thus facilitating safer interventions for cases. In the , the advent of antibiotics in the dramatically reduced infection complications associated with nasal packing, a common treatment that previously carried risks of or due to bacterial colonization. By the 1970s, transcatheter arterial emerged as a for intractable posterior epistaxis, first reported by Sokoloff et al. in 1974, involving selective occlusion of feeding vessels like the to achieve durable with minimal invasiveness. Modern advancements from the 1980s onward incorporated endoscopic techniques, allowing visualization and precise or of bleeding sites, such as the , with success rates exceeding 90% and reduced morbidity compared to open surgery. In the 2010s, clinical trials validated topical as an adjunctive agent, demonstrating faster bleeding cessation and lower rebleeding rates within 24–72 hours when applied intranasally, particularly in anterior epistaxis unresponsive to initial measures.

Terminology origins

The English term "nosebleed" is a compound word derived from "nose" and "bleed," with its earliest recorded use appearing in Middle English texts from the period 1150–1500, reflecting a literal description of blood flowing from the nose. Earlier forms in Old English, such as "nosblod," similarly combined elements meaning "nose" and "blood," emphasizing the straightforward anatomical reference in Anglo-Saxon language. The formal medical term "epistaxis" originates from , combining "epi" (meaning "upon" or "above") and "stazein" (meaning "to drip" or "to let fall in drops"), thus denoting from the as a dripping from above. This term entered English medical literature in the , with the first recorded instance in 1779. Although the word draws from classical Greek roots, it was applied in medical writing by in the 1st century CE, who described nasal hemorrhages in his encyclopedic work De Medicina as part of broader discussions on and surgical interventions. Synonyms for nosebleed include the formal "epistaxis" and the colloquial "bloody nose," the latter a simple descriptive phrase common in everyday English since at least the early modern period. Across cultures, naming reflects traditional medical views; in Traditional Chinese Medicine, nosebleeds are termed "bí nǜ" (鼻衄), associated with "lung heat" where excessive yang heat disrupts blood flow and causes upward flaming of qi. In Arabic medical terminology, the condition is known as "ruʿāf" (رُعَاف), literally denoting nasal bleeding, a term used in classical Islamic texts for both description and treatment discussions. The terminology for nosebleed evolved from superstitious interpretations in , where it was often viewed as an omen of death or divine warning—such as in legends of the Hun choking on a fatal nosebleed on his wedding night, symbolizing impending doom—to a clinical descriptor by the 1800s, as medical advancements shifted focus to anatomical causes like vascular fragility. Up to the , European and Middle Eastern texts treated nosebleeds as a natural purification for internal imbalances, but by the , terms like "epistaxis" became standardized in , emphasizing over mysticism. This transition marked a broader move from humoral and folk explanations to evidence-based nomenclature in Western medicine.