Defn: bleeding from the nose.


-common overall but,

-5% to 10% of patients require otolaryngology review to control the epistaxis.

-Some of these can be a significant challenge to the most experienced physician.

may require hospitalisation, blood transfusions, surgical interruption of nasal blood supply. -If not successfully managed, they can be victims of life-threatening cardiac and respiratory abnormalities and sepsis, which may lead to death.

Anatomy and blood supply:

-Epithelial lining of nasal cavity

Keratinising stratified squamous epithelium lines nasal vestibule

Respiratory epithelium covers septum, floor, and lateral walls

Olfactory epithelium lines superior turbinate and uppermost septum

-Blood supply: is derived from external and internal carotid arteries.

*ECA: (two main branches to nose)

i. maxillary artery in its third (or pterygopalatine) portion gives off several terminal branches:


-enters nasal cavity through sphenopalatine foramen at posterior limit of mid turb

- gives off two branches:

posterior lateral nasal branch (supplies turbinates, ethmoid and maxillary sinuses)

posterior septal branches, (supplies entire septum inferiorly and anteriorly)

descending pharyngeal arteries

ii. facial artery (less significant)

gives off superior labial artery

which gives off - a septal branch to anterior nasal septum and vestibule

- an alar branch to nasal ala


-supplies nose via ophthalmic artery as it arises from the carotid at the cavernous sinus (Fig. 41-1).

-ophthalmic a has two branches:

i. posterior ethmoidal a (smaller of the two)

-enters posterior ethmoidal foramen to supply posterior ethmoid sinus.

-gives off nasal branches which descend through cribriform plate & anastomose with branches of sphenopalatine artery.

ii. anterior ethmoidal a

-enters anterior ethmoidal foramen with nasociliary n & supplies:

- ant ethmoids air cells, frontal sinus, and dura.

- gives off nasal branches which enter nose along crista galli & supply

antero-superior septum and lateral walls.

-areas associated with a high frequency of epistaxis:

-anterior epistaxis occurs in > 90% of cases, (esp in children and young adults).

i. Kiesselbach's or Little's area:

-site of most anterior nosebleeds

-on septum where branches of anterior ethmoidal, sphenopalatine, & sup labial a’s anastomose

ii. Posterior epistaxis: mostly at entry zone of sphenopalatine a behind mid turb


-affects all age groups without sex predilection.

-incidence higher during colder winter months

( due to more frequent URTI’s, & temperature/humidity fluctuations)

-also common in hot dry climates with low humidity.


-Anterior epistaxis is more common in the child or young adult,

-posterior nasal bleeding more common in older adult with hypertension or arteriosclerosis.


-pts who suffer from sinus disease, nasal inflammation, and allergy are more prone to epistaxis because the nasal mucosa is more inflamed, hyperemic, and friable.

-changes from a cold outside environment to a warm, dry, heated house result in changes in the normal nasal cycle of congestion and decongestion.

This Þ poor ventilation of the sinuses,Þ infection, nasal congestion, engorgement of mucosal linings, and ultimately epistaxis.

Any of the following list affecting the nasal cavity, nasopharynx, or sinuses Þ epistaxis

1. Infection -Viral


-Granulomatous (TB, Wegener’s Ganulomatosis, Histoplasmosis, Syphilis)

-Fungal (eg mucormycosis)

2. Inflammatory (eg Atrophic rhinitis)

3. NP Benign (eg polyps, angiofibroma)

Malignant (eg SCC)

4. Trauma: a. Accidental or self-induced

b. Iatrogenic

c. Cocaine

5. Allergy

6. Blood dyscrasias

a. Iatrogenic (drug induced)

b. Disease mediated

c. Alcoholism

7. Congenital (eg Hereditary haemorrhagic telangiectasia or nasal defects)

8. Degenerative (Hypertension & atherosclerotic vascular disease)

Trauma distorts bony cartilaginous framework & tears nasal mucosa

Þ bleeding from raw bone edges or lacerations of vascular mucosa.

Common sites for mucosal tears are along septum, at lateral recesses of the piriform aperture, at junction of upper lateral cartilages with nasal bones, at lateral margins of inf turbinate or at junction of quadralateral cartilage with bone septum.

Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease) an autosomal dominant disease. -inherited lack of contractile elements in the walls of blood vessels.

-the telangiectasias are dilated venules and capillaries or small arteriovenous malformations & are found in the skin or mucosal linings of the entire aerodigestive tract.

-coagulation parameters & platelet function are entirely normal.

-these bleed from the slightest trauma, usually on a daily basis.

Þ recurrent epistaxis GIT haemorrhageÞ hundreds of blood transfusions.

Atrophic rhinitis is caused by a chronic bacterial infection from Klebsiella ozaenae.

Þ Nasal crusting & an atrophic, fibrotic, scarred mucosa.


A. General Measures:

*Calm patient, firmly pinch patient's entire nose ( may stop ant bleeds).

* Sitting preferable b/c ß nasal arterial Press & risk of blood aspiration.

B. Recognise and treat hypovolaemia

- *Look for shock:(feeble pulse, cool/pale skin abN mentation ; etc).

*If significant blood loss, treat for hypovolemia .

*Insert a large-bore (> 16-gauge) intravenous catheter.

*Blood for XM, Hb, clotting factors, EUC’s

*IV infusion of crystalloid solutions

2. Look for underlying cause

*PF’s: H/T, anticoagulants or aspirin, haematology disease.

C. Control of Haemorrhage;

1. Determine the site of bleeding-

*Bright light (headlight or head mirror), nasal speculum, adequate suction device.

*Systematically examine lateral & medial walls of nasal cavity searching for bleeding pts

2. Stop the bleeding-

The site of bleeding varies with the age of patient

a. Children

*Often in Little’s (Kiesselbach's) area, located anteriorly on nasal septum


*usually more posteriorly than Little’s area.

c.Elderly patient

*most difficult

*bleeding source usually high & posterior ( on the lateral wall ).

*It cannot be visualised by conventional rhinoscopy using an anterior approach.

*Calcified arteriosclerotic vessels (inelastic ineffective vasospasm).

*Bleeding can be stopped by:

Chemical (eg silver nitrate) or Electrical cautery, or packing tightly against bleeding point.

Preparing the nose

a.Adequate illumination

b.Suction all visible clot


(i) Cophenylcaine Forte (V/C & L/A)

(ii) Cotton-wool pledgets soaked in either:

-4% lignocaine & adrenaline (max dose 7 mg/kg), or -5% cocaine (max dose i.e. 3 mg/kg)

NB: adequate systemic analgesia (eg morphine)

(i) To perform chemical cautery, use silver nitrate-tipped sticks

*under direct vision , bleeding point only.

- Caution: Do not cauterise wide area of nasal mucosa, and do not cauterise both sides of nasal septum since septal necrosis may result.

(ii)To place an anterior pack,

* Continuous strip of petroleum-impregnated gauze into anterior nares

-Remember floor is horizontal & post choanae are 6 - 7.5 cm deep.

* If bleeding continues, pack other nostril .

*If entire nasal chamber is packed & bleeding persists posteriorly => post pack

(iii)To place a posterior pack,

* Simpson’s balloon or Foley urethral catheter is inserted back along floor of nose, *Inflate balloons (water) & tape catheter to cheek

*Then insert anterior nasal pack

D. After A&E

NBM, IV fluids and antibiotic cover

Routine obs (PR, BP, RR)

Oxygen sat’n monitioring (esp if elderly)

Strict bed rest

TED stockings

Sedation (if no signif resp disease)

Rpt Hb in 6hrs and 24 hrs

NB: A posterior pack should be left in place for 5 days.

Nonsurgical techniques

-conventional packing techniques are associated with 25% failure rate (Montgomery & Reardon 1980)

-When packing fails a procedure to decrease pressure gradient feeding nasal capillary bed is req’d.

-injecting pterygomax space via greater palatine foramen with LA & adrenaline Padrnos (1968)

-cryotherapy to control severe epistaxis (Bluestone and Smith, 1967,in 21 patients).

-proved to be cumbersome, required special equipment, and was less than predictable.

-Angiographic arterial embolization (Robertson & Reardon, 1979) has been used successfully

(esp for posterior epistaxis)

Surgical techniques

-usually the last resort in control of intractable epistaxis.

-early ligation has been advocated due to cost-effectiveness, improved control, and safety.

-Wang and Vogel (1981) found:

-surgical failure rate nearly half that associated with packing (14.3% versus 26.2%),

-decreased local & systemic complication rate with surgery (40% versus 68%),

-average length of hospital stay for surgical patients was 2.2 days < those Rx’d with packing.

1. Anterior and posterior ethmoidal artery ligation

Ind’n: persistent superior and anterior epistaxis

Surgical landmarks:

From Lacrimal Crest:

24mm Ant Ethm

12mm Post Ethm

6mm Optic Nerve

- arteries are ligated vascular hemostatic clips.

2.Management of posterior epistaxis

-Posterior epistaxis not controlled by packing is treated by one of 3 surgical techniques:

(1) external carotid artery ligation,

(2) transantral ligation of maxillary artery,

(3) intra-oral ligation of maxillary artery.

a. Ligation of external carotid artery

-reduces blood flow to capillary bed of nasal mucosa.

-two important points should be made about the procedure:

(1) two branches of ECA must be identified to avoid ligation of ICA;

(2) avoid injury to vagus nerve, superior laryngeal n, hypoglossal n, sympath chain, or

mandibular branch of VII.

-major disadvantages are significant potential exists for collateral blood flow into maxillary a

& injury to above.

b. Transantral ligation of maxillary artery

- first described by Seiffert (1928)

- most widely used arterial ligation procedure to control intractable epistaxis

- Caldwell-Luc procedure to gain access to pterygomaxillary space.


-posterior wall of maxillary sinus is removed to gain access to third part of maxillary artery.

Þ sphenopalatine and greater palatine arteries, are seen & doubly clipped.


-Persistent pain in maxillary dentition, damage to sphenopalatine ganglion and vidian nerve, and oral antral fistula.

-Limitations: not feasible in children, hypoplastic maxillary sinuses, tumors of maxillary sinus, or severely comminuted facial fractures, chronic maxillary sinusitis.

c. Intra-oral ligation of maxillary artery (Maceri & Makielski, 1984)

- provides access to 1st & 2nd parts of maxillary a (as it arises from behind ramus of mandible)

- applicable to all ages, does not require Caldwell-Luc operation,

- can be used in a patient with maxillary fractures as well as cancer patients.


- incision in gingivobuccal sulcus at level of 3rd molar, then inferiorly along ramus of mandible

- blunt dissection of alveolar tissue

- buccal fat pad is retracted medially to enhance exposure.

- temporal muscle belly is split and partially dissected from medial surface of mandible.

- artery is directly visualized at base of the wound

- hemostatic clips are applied

-Probs: varying degrees of trismus for several days or weeks (due to temporal muscle manipulation) potential for damage to inferior alveolar nerve or infection into infratemporal space

Transarterial embolization

-Indicated when adequate packing and arterial ligation have failed to control nasal haemorrhage.

-Angiography before arterial ligation is recommended when there is: (Welsh, 1990):

1. Evidence of flow from the contralateral carotid system

2. Hx of TIA’s, CVA’s physical paresis or paralysis)

3. Vascular compromise of the globe (amaurosis fugax)


-uses computerise digital subtraction angiography to localise bleeding site & define anatomy

-maxillary artery is selectively studied to its most terminal branches.

-material used for embolization can be polyvinyl alcohol spheres (150-590 mm in diameter),

Gelfoam particles, & coil springs.


- direct visualisation of the bleeding site close to the source.

- vessel can be occluded closer to the site of bleeding, (\ ß ‘g effects of collateral blood flow) - success rate of embolization including repeat attempts is 90% (Hicks & Vitek, 1989)

- rapidly performed under LA

- excellent option in patients with bleeding disorders (eg Rendu-Osler-Weber disease)

-Disadv: cannot be used for anterior epistaxis (ie ethmoidal arteries b/c are branches of ICA)

-Complication: < 0.1% (Merland et al., 1980).

- CVA’s & facial nerve paralysis due to ICA embolisation (Metson and Hanson, 1983).

-C/I if: -angiographic evidence of dangerous anastomoses with ICA system,

-severe atheromatous disease,

-allergy to angiographic contrast material.

Other Options:

-use of argon & Nd:YAG laser photocoagulation (Parkin and Dixon 1981)

( neodymium: yttrium aluminum garnet lasers)

-resurfacing nasal septum & lateral walls of nose with dermis obtained from thigh.(Saunders 1968)

(esp in Hered Hemor Telang)


Cummings, C. Otolaryngology. 

Gates G, Current Therapeutics.