Epistaxis

Bleeding from the nasal cavity, affecting up to 60 percent of people at some point, with around 6 percent seeking medical attention and a small proportion requiring admission and intervention. Mortality is essentially confined to elderly patients with posterior bleeds, anticoagulation and cardiovascular comorbidity, in whom aspiration, hypovolaemia and myocardial ischaemia are the mechanisms of death.

Vascular anatomy, which determines management

The nose has a dual supply from both carotid systems.

• Internal carotid, through the ophthalmic artery: anterior and posterior ethmoidal arteries, supplying the superior septum and lateral wall. These cross the ethmoid roof and cannot be embolised safely, since embolisation risks retinal artery occlusion and blindness. Anterior ethmoidal bleeding is controlled surgically.
• External carotid, through the maxillary artery: sphenopalatine artery, which is the dominant supply to the posterior nasal cavity and is the target of endoscopic ligation and of embolisation; and the greater palatine artery.
• External carotid, through the facial artery: superior labial artery supplying the anterior septum and columella.

Little area, on the anteroinferior septum, is the anastomosis of the anterior ethmoidal, sphenopalatine, greater palatine and superior labial arteries, and is the source of around 90 percent of epistaxis. Its superficial position, thin mucosa and exposure to airflow and digital trauma explain this.

Woodruff plexus, on the posterior lateral wall beneath the posterior end of the inferior turbinate, is a venous plexus and a site of posterior bleeding.

Aetiology

Local:

• Digital trauma, which is the commonest cause in children.
• Mucosal drying from low humidity, oxygen therapy and air conditioning.
• Trauma and fracture, including skull base fracture with carotid injury.
• Foreign body, particularly with unilateral foul discharge in a child.
• Rhinitis and rhinosinusitis.
• Septal deviation and perforation.
• Intranasal drugs: corticosteroid sprays with poor technique, decongestants, cocaine.
• Neoplasm: juvenile nasopharyngeal angiofibroma in an adolescent male, inverted papilloma, squamous cell carcinoma, melanoma, esthesioneuroblastoma.
• Postoperative bleeding after sinus, septal or skull base surgery.

Systemic:

• Hypertension, which is associated with epistaxis and makes control harder but is not clearly a primary cause.
• Anticoagulants and antiplatelet agents: warfarin, direct oral anticoagulants, heparin, aspirin, clopidogrel, and dual antiplatelet therapy.
• Coagulopathy: haemophilia, von Willebrand disease which is the commonest inherited bleeding disorder, thrombocytopenia, liver disease, chronic kidney disease with platelet dysfunction.
• Hereditary haemorrhagic telangiectasia, an autosomal dominant condition with mucocutaneous telangiectases, recurrent epistaxis in over 90 percent, and visceral arteriovenous malformations in the lung, liver and brain.
• Haematological malignancy.
• Vasculitis and granulomatous disease.

• Anterior bleeding: visible bleeding from the nostril, usually unilateral, from Little area, typically in younger patients, and generally controllable with simple measures.
• Posterior bleeding: bleeding predominantly into the pharynx, often bilateral, with the patient swallowing or spitting blood, occurring in older patients, more profuse, harder to control, and more likely to require intervention.
• Haematemesis and melaena from swallowed blood, which mislead the unwary into investigating an upper gastrointestinal source.
• Dizziness, palpitations, pallor and syncope in significant blood loss.
• Airway compromise from aspiration, which is the immediate threat in a profuse posterior bleed.

Assessment priorities

• Estimate blood loss, which is almost always underestimated, since much is swallowed.
• Vital signs: tachycardia, hypotension, and postural change. In the elderly on beta blockers, tachycardia may be blunted.
• Duration, frequency, laterality and previous episodes.
• Anticoagulant and antiplatelet use, and specifically the last dose and the indication, including mechanical heart valve or recent stent, which restrict reversal.
• Bleeding history: bruising, gum bleeding, menorrhagia, family history.
• Trauma, surgery and drug use.
• Ask about telangiectases on lips, tongue and fingers, and family history of recurrent epistaxis, for hereditary haemorrhagic telangiectasia.

• Full blood count, group and save or crossmatch depending on severity, coagulation screen, renal function and liver function.
• International normalised ratio in warfarinised patients. Note that direct oral anticoagulants are not reliably assessed by standard coagulation tests; anti Xa assays for apixaban and rivaroxaban, and thrombin time or dilute thrombin time for dabigatran, are needed where available.
• Examine with a good light source, head light, nasal speculum and suction after the patient blows out clots and after topical decongestion and anaesthesia. Adequate examination is impossible with blood and clot in situ and this step is regularly omitted.
• Rigid nasal endoscopy after decongestion, which identifies the bleeding point in the great majority including many posterior points, and is the single most useful diagnostic step. It converts blind packing into targeted cautery.
• Computed tomography angiography for suspected traumatic vascular injury, pseudoaneurysm of the internal carotid after skull base trauma or surgery, or where a vascular tumour is suspected.
• Contrast enhanced computed tomography or magnetic resonance imaging where a mass is seen or suspected, and never biopsy a suspected angiofibroma in an adolescent male without imaging first.
• Investigate recurrent unexplained epistaxis for coagulopathy, and consider von Willebrand screening in young patients with a suggestive history.
• Investigate for hereditary haemorrhagic telangiectasia using the Curaçao criteria: spontaneous recurrent epistaxis, mucocutaneous telangiectases, visceral arteriovenous malformations, and a first degree relative with the condition. Three criteria are definite, two are possible.

Manage in a stepwise fashion, escalating only when the previous step fails. Resuscitate in parallel with controlling bleeding.

Immediate first aid and resuscitation

• Sit the patient upright, leaning forward, to reduce venous pressure and prevent aspiration.
• Pinch the soft cartilaginous part of the nose, not the bony bridge, continuously for 10 to 15 minutes without releasing to check. This alone controls the majority of anterior bleeds and is done incorrectly by most patients.
• Ask the patient to spit out blood rather than swallow it, so loss can be estimated and vomiting avoided.
• Ice pack to the bridge or an ice cube sucked in the mouth, which produces reflex vasoconstriction.
• Two large bore cannulae, bloods, and fluid resuscitation with crystalloid where there is haemodynamic compromise. Transfuse according to haemodynamic status and haemoglobin, with a threshold generally around 70 g/L, or 80 g/L in patients with ischaemic heart disease.
• Oxygen, cardiac monitoring and airway protection in profuse posterior bleeding. Involve anaesthetics early where aspiration is a risk.
• Reverse coagulopathy as below.

Topical preparation and cautery

• Apply pledgets soaked in a vasoconstrictor and anaesthetic: cocaine 4 to 5 percent, or lidocaine 5 percent with phenylephrine 0.5 percent, or lidocaine 2 percent with adrenaline 1 in 10000, left in place for 5 to 10 minutes. Cocaine is contraindicated in ischaemic heart disease, uncontrolled hypertension and pregnancy.
• Topical tranexamic acid, applied on a soaked pledget or as a soaked gauze at 500 mg in 5 mL, is effective and reduces the need for packing.
• Silver nitrate cautery of the identified bleeding point, applied to the surrounding area first and then the point itself, for no more than 5 to 10 seconds. Never cauterise both sides of the septum at the same site or at the same visit, since this causes septal perforation.
• Electrocautery or suction diathermy under endoscopic vision for posterior points, which is highly effective and avoids packing.

Nasal packing

Used when the bleeding point cannot be identified or cautery fails.

• Anterior packing with an expandable sponge such as Merocel, an inflatable balloon device such as Rapid Rhino with a carboxymethylcellulose coating which is more comfortable and promotes platelet aggregation, or ribbon gauze impregnated with bismuth iodoform paraffin paste for the largest bleeds.
• Insert along the nasal floor, parallel to the hard palate, not upward toward the bridge, which is the commonest technical error and causes pain without controlling bleeding.
• Bilateral packing may be required for a septal bleed, since unilateral packing simply diverts the bleeding.
• Posterior packing with a double balloon device or a Foley catheter passed to the nasopharynx, inflated with 5 to 10 mL of saline, withdrawn until it engages the choana and then secured with an anterior pack. Never use air in the posterior balloon, and always protect the columella and alar rim from pressure necrosis with padding.
• Any patient with a posterior pack requires admission, cardiac monitoring and observation, since the nasopulmonary reflex causes hypoxia and arrhythmia in elderly patients, and mucosal pressure necrosis occurs.
• Dissolvable haemostatic agents such as oxidised cellulose, gelatin thrombin matrix and chitosan based dressings are useful in coagulopathic patients where removal of a traditional pack would cause rebleeding.
• Packs are removed at 24 to 48 hours, and prolonged packing beyond 48 to 72 hours increases infection, sinusitis and necrosis.
• Antibiotic prophylaxis with packing is commonly given, using co amoxiclav 625 mg three times daily, though evidence for prevention of toxic shock syndrome is weak. Where used, it should be for packs remaining beyond 48 hours or in immunocompromised patients.

Reversal of anticoagulation

• The decision to reverse balances bleeding severity against thrombotic risk, and should involve haematology in patients with mechanical valves, recent venous thromboembolism or recent coronary stents.
• Most epistaxis in anticoagulated patients is controlled locally without reversal, and reversal should not be reflexive.
• Warfarin with major bleeding: vitamin K 5 to 10 mg intravenously plus four factor prothrombin complex concentrate dosed by weight and international normalised ratio, typically 25 to 50 units/kg. For minor bleeding with a supratherapeutic international normalised ratio, withhold warfarin and give vitamin K 1 to 3 mg orally.
• Direct oral anticoagulants: withhold the drug, and for life threatening bleeding use idarucizumab 5 g intravenously for dabigatran, or andexanet alfa for apixaban and rivaroxaban where available, or prothrombin complex concentrate 50 units/kg where it is not. Note the short half lives, so time and supportive care are often sufficient.
• Antiplatelets: platelet transfusion for life threatening bleeding, and consider desmopressin 0.3 micrograms/kg in uraemic platelet dysfunction.
• Tranexamic acid 1 g intravenously or orally three times daily, which reduces rebleeding. Avoid in patients with a history of thromboembolism and in haematuria from an upper renal tract source.

Surgical and radiological intervention

Indications: failure of adequate packing, recurrent significant bleeding, and haemodynamic instability.

• Endoscopic sphenopalatine artery ligation with clips or diathermy, performed at the sphenopalatine foramen behind the posterior end of the middle turbinate. Success rates of 90 to 95 percent, low morbidity, and it is now the procedure of choice, replacing maxillary artery ligation and external carotid ligation. Identify and control all branches, since a missed branch is the usual cause of failure.
• Anterior ethmoidal artery ligation through a Lynch incision or endoscopically, for superior bleeding, bleeding after trauma, and where sphenopalatine ligation has failed. The artery is found on the frontoethmoidal suture line, approximately 24 mm from the anterior lacrimal crest, with the posterior ethmoidal artery a further 12 mm posteriorly and the optic nerve 6 mm behind that.
• Embolisation of the sphenopalatine and internal maxillary arteries, with success rates of 85 to 95 percent. It is useful in patients unfit for general anaesthesia and in hereditary haemorrhagic telangiectasia. Complications include stroke, facial pain, trismus, facial nerve palsy, skin necrosis and, rarely, blindness. Ethmoidal arteries must not be embolised.
• Septal surgery where a spur or deviation causes recurrent bleeding.

Specific situations

• Juvenile nasopharyngeal angiofibroma: an adolescent male with unilateral obstruction and recurrent severe epistaxis. Diagnose with contrast computed tomography and magnetic resonance imaging showing the characteristic widening of the sphenopalatine foramen and pterygopalatine fossa. Never biopsy. Manage with preoperative embolisation 24 to 48 hours before endoscopic or open resection.
• Hereditary haemorrhagic telangiectasia: humidification, emollients, topical tranexamic acid, oral tranexamic acid 1 g three times daily, and avoidance of packing where possible since it damages further mucosa. Laser photocoagulation with potassium titanyl phosphate or neodymium yttrium aluminium garnet, sclerotherapy, bevacizumab given topically, by submucosal injection or systemically, and in refractory disease Young procedure with surgical closure of the nasal vestibules, which is highly effective but eliminates nasal breathing. Screen for pulmonary and cerebral arteriovenous malformations and provide antibiotic prophylaxis for procedures.
• Post traumatic epistaxis with skull base fracture, where a carotid pseudoaneurysm must be excluded with angiography if bleeding is delayed, profuse and recurrent.

Prevention and follow up

• Nasal emollient such as petroleum jelly or an antiseptic cream applied to Little area twice daily for 2 to 4 weeks, which reduces recurrence.
• Naseptin cream containing chlorhexidine and neomycin twice daily for 10 days reduces recurrence in children, but is contraindicated in peanut and soya allergy given the arachis oil base.
• Humidification, avoidance of nose picking, correction of nasal spray technique.
• Control hypertension.
• Avoid hot drinks, hot baths, alcohol, straining and heavy lifting for 24 to 48 hours after an episode.
• Follow up with endoscopy in adults with unilateral recurrent epistaxis to exclude neoplasm, and investigate recurrent unexplained epistaxis for coagulopathy.