bubble_chart Overview

Epistaxis, also known as nosebleed, is the most common pathological bleeding in humans and a frequent condition in otolaryngology. It can be caused by lesions within the nasal cavity itself or by disorders in the surrounding nasal area or even systemic sexually transmitted diseases. Therefore, comprehensive consideration is necessary during treatment.

bubble_chart Etiology

The nasal mucosa contains a rich vascular bed and is in direct contact with the external environment, so there are many causes of epistaxis. For convenience of description, they are now divided into two categories: local causes and systemic causes:

I. Local Causes

1. Nasal mucosal ulcers and erosions: Commonly seen in the anterior inferior region of the nasal septum (Little's area), often caused by chronic inflammation. Chemical gases, high temperatures, and dry air can all be contributing factors. In addition, nasal septal spurs or ridges, nasal septal perforations, and atrophic rhinitis can also lead to localized nasal mucosal ulcers and subsequent bleeding.

2. Acute infections of the nose and sinuses.

3. Trauma: Traumatic injury of the nose resulting in tearing of the nasal mucosa can cause epistaxis. Fractures of the naso-orbital-ethmoid complex often complicate with rupture of the anterior ethmoidal artery, leading to bleeding in the upper nasal cavity. Skull base fractures may rupture the internal carotid artery, forming a traumatic pseudoaneurysm, which can cause severe epistaxis through the sphenoid sinus. Fractures of the anterior cranial fossa with rupture of the anterior cerebral artery may result in bleeding at the horizontal plate of the ethmoid bone in the roof of the nasal cavity.

4. Tumors: Epistaxis caused by tumors is usually due to ulceration of the tumor surface, with the severity of bleeding varying depending on the nature of the tumor. In advanced stages, malignant tumors invading major blood vessels can lead to fatal epistaxis.

(1) Benign tumors: The most severe is nasopharyngeal angiofibroma, which mostly occurs in young males. Next is hemorrhagic nasal polyps. Capillary hemangiomas in the nasal cavity and sinuses are also relatively common causes of bleeding.

(2) Malignant tumors: Such as nasopharyngeal carcinoma, primary adenocarcinomas, squamous cell carcinomas, melanomas, and sarcomas of the nasal cavity and sinuses. In the early stages, bleeding may only manifest as blood-tinged nasal discharge or bloody mucus, but injury to larger blood vessels can result in severe epistaxis.

II. Systemic Causes

1. Increased venous pressure in the head and neck: Seen in conditions such as chronic bronchitis, pulmonary emphysema, cor pulmonale, and congestive heart failure. When patients cough, the venous pressure in the head and neck rises, easily causing dilation and rupture of the Woodruff venous plexus at the posterior end of the inferior nasal meatus, leading to bleeding. Sometimes, elderly patients straining due to constipation can also cause epistaxis.

2. Increased fragility of blood vessel walls: Seen in conditions such as arteriosclerosis and deficiencies of vitamins C and K. Picky eating leading to deficiencies in vitamins and certain trace elements is a common cause of epistaxis in children. Additionally, chronic gastrointestinal diseases and liver diseases can also result in vitamin deficiencies.

3. Hereditary hemorrhagic telangiectasia (Osler's disease): In this condition, the endothelial cell junctions between peripheral small arteries and veins lack elastic fibers and dilate irregularly. The most common site of bleeding is the vascular plexus in the anterior nasal septum.

4. Blood coagulation disorders: Any hematologic disease affecting the coagulation mechanism can cause epistaxis, which may sometimes be the initial symptom of these diseases. Common examples include aplastic anemia, leukemia, thrombocytopenic purpura, allergic purpura, and hemophilia. The characteristic feature of epistaxis in hematologic diseases is widespread bleeding sites, often involving mucous membranes and skin throughout the body, with epistaxis being prolonged and recurrent. Additionally, liver diseases impairing the synthesis of prothrombin and fibrin can also lead to epistaxis.

5. Others: Wind-damp-heat, acute febrile epidemic diseases (such as typhoid fever and relapsing fever), hyperthyroidism, and epistaxis during menstruation. Long-term use of large doses of nonsteroidal anti-inflammatory drugs like aspirin and indomethacin can also cause epistaxis by affecting arachidonic acid metabolism and impairing thromboxane formation.

6. Rapid changes in atmospheric pressure: Such as during flying, diving, or high-altitude reactions, can also lead to epistaxis.

bubble_chart Diagnosis

For patients with nosebleeds, a comprehensive and precise examination should be conducted, as it is crucial for the effectiveness of future treatment.

1. **Medical History Inquiry** In severe cases of nosebleeds, patients often present with bloodstains on both sides. By inquiring about the medical history, the side that first bled can be identified, which is likely the bleeding nostril. Understanding any major related diseases in the past is also necessary.

2. **Quickly Locate the Bleeding Site** Place a cotton pad soaked in 0.1% adrenaline into the bleeding nostril. Remove it after one minute and examine the nasal cavity to locate the bleeding site.

(1) **Anterior-Inferior Nasal Septum** The nasal mucosa in this area contains branches from the anterior ethmoidal artery, nasopalatine artery, and superior labial artery, which form a network in the superficial layer of the mucosa. This region is called the Kiesselbach area or Little’s area and is a common site of bleeding.

(2) **Base of the Anterior Nasal Septum** If there is pulsatile bleeding in this area, apply finger pressure to the upper lip on the same side. If the bleeding reduces or stops, it indicates a rupture of the nasal septal branch of the superior labial artery. In treatment, ligation of the superior labial artery may need to be considered.

(3) **Top of the Nasal Cavity** In cases of head or facial trauma, the top of the nasal cavity should be examined. Blood flowing down from the top suggests a rupture of the anterior ethmoidal artery. The anterior ethmoidal artery runs through the ethmoid sinus air cells, and severe bleeding can occur if the ethmoid sinus is fractured.

(4) **Severe Nosebleed Days After Head Trauma** If severe nosebleeds occur days after head trauma, the patient’s vision and extraocular muscle function should be checked to rule out middle cranial fossa fracture or a pseudoaneurysm caused by rupture of the internal carotid artery.

**Diagnostic Criteria for Internal Carotid Pseudoaneurysm:**

① History of head trauma. ② Decreased vision or blindness. ③ Oculomotor nerve palsy. ④ Profuse nosebleed after a latent period. ⑤ Intracranial vascular bruit. ⑥ Intracranial angiography.

(5) **Nasal Endoscopy** If bleeding occurs behind a deviated nasal septum, at the posterior edge of the nasal septum, behind the middle turbinate, at the anterior or posterior end of the inferior turbinate, or on the nasal floor or walls, a nasal endoscope can be used to pinpoint the exact bleeding site.

3. **If time permits, perform a sinus X-ray.**

4. **For severe nosebleeds, quickly assess the patient’s overall condition.**

(1) Check temperature, pulse, heart function, blood pressure, and perform a complete blood count.

(2) Observe the skin, conjunctiva, and oral mucosa for signs of bleeding or bruising to determine if there is a blood disorder.

(3) For unconscious patients with nosebleeds, monitor for frequent swallowing movements. An oropharyngeal examination must be performed to assess whether the bleeding is continuing and flowing into the stomach via the pharynx.

bubble_chart Treatment Measures

The treatment principle for nosebleeds should be "address the symptoms first, then the root cause," meaning to stop the bleeding as quickly as possible before proceeding with disease cause treatment. From a treatment perspective, nosebleeds can be divided into two main categories: minor bleeding and sudden severe bleeding.

I. Minor Bleeding

  For this type of epistaxis, the bleeding point should first be identified. Due to the small amount of bleeding, there is ample time to carefully locate the bleeding site. After identifying the bleeding area with a general nasal speculum, the treatment methods are as follows:

1. Cauterization  The nasal mucous membrane at the bleeding site is anesthetized, and 50% silver nitrate or trichloroacetic acid is applied to coagulate the proteins and seal the ruptured small blood vessels. Electrocautery, laser therapy, or cryotherapy can also be used.

2. Submucosal Dissection  For cases of recurrent bleeding from the anterior nasal septum mucous membrane, this method can be employed. The procedure is the same as a conventional submucosal septal resection. If the nasal septum cartilage is deviated, it should be removed, and the dissection range should be slightly wider. Narwla (1987) suggested, based on a study, that this method is superior to ligating the stirred pulse, possibly because some cases actually involve a deviated nasal septum or because the submucosal vascular network is sufficiently disrupted.

3. Scar Formation  The nasal mucous membrane is anesthetized, and three incisions, each 1–1.5 cm long, are made in the prone bleeding area of the nasal septum using an ophthalmic triangular knife. The mucous membrane is incised to sever the dilated capillaries, and a 1–2 mm wide submucosal dissection is performed on both sides of the incisions, followed by compression for 24 hours.

4. Endoscopic Electrocautery  If the bleeding point is difficult to locate with an anterior nasal speculum, nasal endoscopy can be performed to identify posterior bleeding sites, such as the posterior nasal septum, the posterolateral wall of the inferior nasal meatus, the posterior nasal floor, or the middle nasal meatus. Under endoscopy, an electrocautery probe is introduced to cauterize the area, or laser cauterization can be performed via optical fibers. Since CO₂ and YAG lasers can cause extensive burns, the KTP laser is more suitable. The area around the bleeding point should be cauterized first, followed by the severed blood vessel ends.

II. Sudden Severe Bleeding

  This type of epistaxis is often rapid and severe, making immediate hemostasis crucial before further investigating the disease cause for treatment. The main hemostatic measures include:

1. Anterior Nasal Packing  This is the primary method for treating severe epistaxis. The packing material is sterile Vaseline gauze. A hard plastic nasal tube should be placed beforehand to maintain minimal nasal airflow, especially important for bilateral nasal packing. Nasal packing is typically left in place for 24 hours and then removed in one or multiple stages to avoid sinus or middle ear complications. If the packing needs to remain for several days or even a week, antibiotic powder should be added to the packing, or iodoform gauze can be used. Vaseline gauze packing is quite painful for patients, so improved methods include:

(1) Hemostatic Sheath Packing  An oil-coated finger cot or rubber sheath is first placed in the nasal cavity, followed by gauze packing inside the sheath.

(2) Balloon Compression Hemostasis  A rubber or silicone membrane balloon with a ventilation tube is placed at the nasal bleeding site. The balloon is inflated to compress the bleeding area while maintaining nasal breathing through the ventilation tube.

2. Posterior Nasal Packing  If bleeding persists into the throat or the opposite nostril after anterior nasal packing, it indicates a posterior nasal bleeding site, requiring posterior nasal packing. Posterior nasal packing should not be left in place for too long, typically removed within 24–36 hours to avoid complications such as skull base osteomyelitis or meningitis. The main packing material is a conical gauze ball. Nowadays, balloon compression with a ventilation tube is preferred, as it significantly reduces patient discomfort and lowers the risk of complications.

First, spray a topical anesthetic on the affected side of the nasal cavity and pharynx. Insert a thin catheter through the anterior nostril into the nasal cavity, passing along the nasal floor through the posterior nasal aperture to the oropharynx. Use a hemostat to pull the tip of the catheter out of the mouth, leaving the tail end outside the anterior nostril. Then, tie the prepared sterile Vaseline gauze ball (a conical gauze ball slightly thicker than a thumb) with double threads to the front end of the catheter. Pull the tail end of the catheter back from the anterior nostril, causing the gauze ball to move from the oral cavity backward and lodge in the pharynx. Quickly use a hemostat to push the gauze ball upward into the nasopharynx while simultaneously pulling the tail end of the catheter outward from the nostril to tighten it, ensuring the gauze ball blocks the posterior nasal aperture on the affected side. Do not loosen the double threads exposed at the anterior nostril. Proceed with anterior nasal packing, then place a dry gauze ball at the anterior nostril and tie the double threads around it to prevent the posterior nasal packing gauze ball from slipping downward. Guide the double threads hanging from the gauze ball in the pharynx out through the mouth to the cheek and secure them with adhesive tape, leaving them for downward traction when removing the gauze ball two days later.

For sudden epistaxis, repeated packing will inevitably injure the nasal mucosa, leading to increasingly severe bleeding. In such cases, absorbable packing materials can be used. After a single packing, no further removal or replacement is needed. The packing material will liquefy and be absorbed or expelled naturally within a week. Such materials include gelatin sponge, oxidized cellulose, and fibrin foam (fibrinfoam). Before use, they should be soaked in a coagulant solution, and excess liquid should be squeezed out before packing into the nose.

Nasal packing remains the primary method for treating epistaxis. The success rate of anterior nasal packing exceeds 90%, while combined anterior and posterior nasal packing ranges between 48% and 80%. Monux (1990) reported a 100% success rate in hemostasis among 322 cases of nasal packing. Although packing is effective, its complications should not be overlooked, especially in elderly patients and those with poor cardiac or pulmonary function. Severe reactions such as myocardial infarction or death may occur. Therefore, close monitoring of cardiac and pulmonary function is essential for such patients after nasal packing.

3. Vascular Ligation If nasal packing fails to effectively stop bleeding, vascular ligation should be performed. This is generally divided into extravascular and intravascular treatments.

(1) External Carotid Artery Ligation The blood vessels below the level of the middle turbinate in the nasal cavity are terminal branches of the external carotid artery. Ligation can achieve a certain hemostatic effect.

The patient is placed in a supine position with the shoulder elevated and the head turned to the opposite side. Infiltration anesthesia is administered along the anterior border of the sternocleidomastoid muscle. With the superior cornu of the thyroid cartilage as the midpoint, an incision is made along the anterior border of the sternocleidomastoid muscle through the skin and subcutaneous tissue. The sternocleidomastoid muscle is retracted posteriorly to expose the common carotid artery and its internal and external branches. The external carotid artery is then dissected upward to reveal the superior thyroid artery and the lingual artery above it. The posterior belly of the digastric muscle and the hypoglossal nerve in the upper part of the incision are retracted upward. A thick silk thread is passed around the external carotid artery between the superior thyroid artery and the lingual artery using an aneurysm needle and ligated. At this point, the superficial temporal artery should cease pulsating, which serves as an indicator of successful ligation.

Carotid artery anomalies can complicate the surgery. The following four special situations require careful handling:

① In more than half of cases, the bifurcation of the common carotid artery is above the level of the superior border of the thyroid cartilage. A standard incision may only expose the common carotid artery without revealing the external carotid artery. Care must be taken to avoid mistakenly ligating the common carotid artery. In such cases, the incision should be extended upward to expose the posterior belly of the digastric muscle and the stylohyoid muscle. The parotid gland is retracted upward, and the external carotid artery is located deep within the parotid gland and ligated. During dissection and retraction of the parotid gland, care should be taken to avoid injuring the facial nerve.

② The superior thyroid artery may sometimes arise directly from the common carotid artery. In such cases, further upward dissection is needed to locate the bifurcation of the common carotid artery and distinguish between the internal and external carotid arteries. The external carotid artery gives off the lingual artery, while the internal carotid artery has no branches. This prevents mistaking the common carotid artery above the superior thyroid artery for the external carotid artery and erroneously ligating the common carotid artery.

③ The external carotid artery may sometimes lie posterior to the internal carotid artery. In such cases, judgment should not be based solely on anatomical position but strictly on the presence or absence of branches. Only after clearly identifying the superior thyroid artery and the lingual artery should ligation be performed to avoid mistakenly ligating the internal carotid artery.

④ The superior thyroid artery may sometimes be absent or merge with the lingual artery into a single branch. In such cases, as long as the bifurcation of the common carotid artery is identified, the external carotid artery can be safely ligated without the risk of mistakenly ligating the internal carotid artery.

During dissection of the common carotid artery bifurcation, 1% novocaine should be instilled into the carotid sheath to prevent carotid sinus reflex.

Common carotid artery ligation is only applicable for epistaxis caused by traumatic internal carotid artery aneurysms. During the operation, care should be taken to avoid injuring the vagus nerve. However, common carotid artery ligation will inevitably reduce the blood supply to the brain tissue. For safety reasons, it is best to perform an adaptation test before ligation, which involves compressing the common carotid artery with a finger for 10 minutes to observe whether the patient exhibits any electroencephalogram changes or positive neurological signs. This method is called the Matas test. If there are no adverse reactions, ligation can proceed.

Clinically, it has been observed that after ligation of the external carotid artery, collateral circulation is rapidly established, and the hemostatic effect is sometimes not durable. Therefore, recent practice tends to favor ligation of the distal vessels.

(2) Internal maxillary artery ligation Since the blood supply to the nasal cavity mainly comes from the internal maxillary artery, ligation should be most effective. The approach can be via the maxillary sinus or intraorally.

① Maxillary sinus approach First reported by Seiffert (1928) and later popularized by Chandler et al., this approach follows the conventional radical maxillary sinusotomy, but the gingivobuccal incision should be slightly longer, and the anterior wall window should be slightly larger. When removing the posterior wall of the sinus, the excavation should be extended as medially as possible. After incising the posterior wall periosteum and entering the pterygopalatine fossa, use forceps to dissect the adipose tissue. Upon identifying a transverse vein, the internal maxillary artery can be found 4–5 mm deeper. Vascular clips are then placed at the following three sites: the distal end of the internal maxillary artery, the distal end of the descending palatine artery, and the proximal end near the main trunk of the internal maxillary artery.

② Intraoral approach In cases of severe maxillary bone injury, tumor filling the maxillary sinus, acute maxillary sinusitis, or poor maxillary sinus pneumatization, the intraoral approach may be chosen. This method was first introduced by Maceri (1984). An incision is made in the oral mucosa at the level of the second and third molars, extending across the buccogingival groove to the mandibular ramus. The buccal fat pad is appropriately dissected and removed, the incision is slightly widened, and a finger is inserted for blunt dissection to identify the mandibular ramus and the attachment of the temporalis muscle. The temporalis muscle is dissected while preserving its lower attachment. The internal maxillary artery can then be palpated between the lateral aspect of the mandibular ramus and the medial side of this muscle. After identifying the vessel, two vascular clips are placed distally and one proximally. The fat pad is repositioned, and the incision is sutured. This method primarily involves incising the buccal fat pad and ligating the internal maxillary artery posterior to the maxilla before it enters the pterygopalatine fossa and branches. However, the depth of the internal maxillary artery beneath the oral mucosa varies, ranging from 12 mm superficially to 40 mm deeply.

(3) Anterior ethmoidal artery ligation This is indicated for traumatic epistaxis in the upper nasal cavity or ethmoid sinus, or for cases where epistaxis persists despite internal maxillary artery ligation. This is because after occlusion of the internal maxillary artery, blood from the internal carotid artery may supply the external carotid artery branches of the nose via anastomoses.

A curved incision is made between the medial canthus of the affected side and the midline of the nasal root, extending superiorly to the eyebrow and inferiorly to the level of the medial canthus, down to the periosteum. The periosteum is dissected along the orbital wall, and at a depth of 2–3 cm, the sheath of the anterior ethmoidal artery can be seen traversing toward the anterior ethmoidal foramen. The artery is isolated and ligated or coagulated with bipolar electrocautery.

(4) Superior labial artery ligation This is suitable for severe bleeding in the anterior inferior nasal cavity that persists despite packing, where digital compression of the affected anterior naris reduces bleeding, indicating bleeding from the terminal branches of the superior labial artery. Inject 1–2 ml of 1% procaine 0.5 cm below the anterior naris and infiltrate the nasal vestibule. A suture needle is inserted 0.5 cm below the anterior naris, passed upward to the base of the nasal vestibule at a depth of about 0.5 cm, and then tied below the anterior naris.

(5) Pterygopalatine fossa injection This method involves injecting a certain volume of medication into the pterygopalatine fossa, a closed space filled with adipose tissue, to compress the vessels within the fossa, reduce blood flow to the nasal mucosa, and occlude the vessels to achieve hemostasis. The injection can be administered via the greater palatine foramen. The distances from the greater palatine foramen to the sphenopalatine foramen, foramen rotundum, inferior orbital fissure, and optic canal are all 2.6 cm or more. The greater palatine canal angles 60°–80° posteriorly and superiorly relative to the hard palate plane. A 4 cm-long dental anesthesia needle is bent 60° at 2.5 cm from the tip to prevent excessive penetration into the orbit or cranial cavity. A solution of 2% lidocaine with 0.1% adrenaline (2–3 ml) is injected within half a minute. Alternatively, 5–10 ml of 0.25% procaine can be injected directly into the pterygopalatine fossa through the cheek skin.

For patients with severe bleeding after nasal packing or maxillary artery ligation, maxillary artery embolization can be performed. This method involves inserting a 5F catheter through the ipsilateral femoral artery or common carotid artery puncture into the external carotid artery on the bleeding side, then guiding it into the maxillary artery under fluoroscopy. Angiography is first performed to confirm the absence of communicating branches with the internal carotid artery or ophthalmic artery. If no major communicating branches are present, 1mm×3mm gelatin sponge particles mixed with 50% saline and 50% contrast agent can be slowly injected into the maxillary artery until its branches are no longer visible under fluoroscopy. The pressure during gelatin sponge injection should be as gentle as possible to prevent reflux of gelatin sponge particles in case of obstruction, which could lead to accidental entry into the internal carotid artery and cause cerebral embolism. After embolization, observe for 15 minutes; if there is no bleeding, withdraw the catheter.

III. Internal carotid artery rupture causing severe epistaxis

Skull base fracture leading to internal carotid artery rupture and bleeding, forming a pseudoaneurysm, which may bleed again when reaching a certain size, with blood flowing into the nasal cavity through the sphenoid sinus. For such nasal bleeding, anterior and posterior nasal packing should be performed first, followed by the following treatments:

1. Isolation of the pseudoaneurysm First, ligate the common carotid artery and external carotid artery on the affected side, then perform a craniotomy in the anterior cranial fossa on the affected side. Use a Scoville clip to occlude the internal carotid artery proximal to the pseudoaneurysm. If necessary, ligate the ophthalmic artery as well. This cuts off the blood supply to the pseudoaneurysm, completely isolating it and achieving hemostasis.

2. Muscle packing hemostasis in the sphenoid sinus Make an external nasal incision and open the sphenoid sinus via the ethmoid sinus. Inspect the impression of the internal carotid artery on the superolateral wall of the sphenoid sinus, aspirate blood clots from the sinus, and tightly pack the area with autologous muscle to compress the rupture site of the internal carotid artery. Strict aseptic techniques must be followed to prevent intracranial infection.

3. Detachable balloon embolization Under X-ray fluoroscopy, perform arterial puncture and guide the arterial catheter to the rupture site of the internal carotid artery. Use a detachable balloon to embolize the site. After inflating the balloon to compress the area and achieve hemostasis, leave the balloon in place and withdraw the catheter. This method is highly effective and avoids craniotomy.

For epistaxis caused by other diseases, the primary focus should be treating the underlying condition, such as cardiovascular diseases, liver diseases, or hematologic disorders. Epistaxis due to tumors or inflammatory granulomas in the nasal sinuses or nasopharynx should also be managed by treating the primary disease. In cases of sudden massive bleeding from nasopharyngeal angiofibroma, perform a tracheostomy first, followed by anterior and posterior nasal packing to buy time for surgical preparation.

Patients with hereditary hemorrhagic telangiectasia often experience recurrent and sometimes severe epistaxis. A preferred treatment involves dissecting and excising the nasal septum and floor mucosa, followed by autologous free skin grafting to cover the wound, secured with sutures. Fascia may also be used as an alternative to free skin grafts.

IV. Systemic treatment for epistaxis

1. Blood transfusion and fluid replacement The decision should be based on the amount of blood loss. If the patient exhibits hypotension, pallor, sweating, or lethargy, a blood transfusion is necessary. If nasal packing interferes with eating or if significant vomiting occurs due to swallowed blood, administer fluids promptly to replenish electrolytes.

2. Use of hemostatic agents These may be administered after implementing the aforementioned hemostatic measures, though their efficacy in treating epistaxis remains uncertain. Recently, Vinayak et al. (1993) reported satisfactory results with intravenous glypressin for acute epistaxis.

3. Treatment of the underlying disease etiology.