Epistaxis

Anatomical Types:

From a clinical perspective, bleeding will be either from the lateral nasal wall or from the septum.

Lateral nasal wall bleeding: (mostly posterior)

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Most major bleeds that occur without trauma will be posterior.

Sphenopalatine artery, which enters through the sphenopalatine foramen at the posterior end
of the middle turbinate.

Almost immediately after exiting the foramen, the sphenopalatine artery gives off the posterior
nasal artery. This artery supplies branches to the superior turbinate before passing above the
posterior bony choana on the anterior face of the sphenoid sinus to the posterior aspect of the
septum. This vessel may be cut if the natural ostium of the sphenoid sinus is enlarged inferiorly
and can result in an impressive arterial bleeder during surgery.

The other potentially vascular area on the lateral nasal wall is the region under the posterior
end of the inferior turbinate where the sphenopalatine artery and posterior pharyngeal artery
may anastomose and is termed Woodruff's area.

Septal bleeding: (mostly anterior)

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Responsible for the majority of nose bleeds (95%).

Septum is supplied by the posterior nasal artery, the greater palatine artery (through the incisor
foramen), the anterior and posterior ethmoidal arteries, and branches of the labial artery
entering the nose anteriorly. These vessels tend to anastomose in the region about 1.5 cm behind
the anterior mucocutaneous junction, which is termed either Little's area or Kiesselbach's
plexus.

Etiology:
Local
Trauma: digital, fractures
Nasal sprays (local trauma effect)
Inflammatory reactions
Anatomic deformities (e.g., septal spur/deflection)
Foreign bodies
Intranasal tumors
Chemical irritants
Nasal prong O2, CPAP
Surgery
CPAP, continuous positive airway pressure.

Systemic
Hypertension
Vascular disorders
Blood dyscrasias
Hematologic malignancies
Allergies
Malnutrition
Alcohol
Drugs
Infections

Blood dyscriasis:

Heriditary disorders:
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The most common inherited bleeding diatheses are:

1. von Willebrand disease, the most common inherited bleeding diatheses, with reduction in
von Willebrand factor (vWF). The procoagulant factor and vWF together form factor VIII.
2. Hemophilia A, with a reduction of procoagulant factor of factor VIII.
3. Heophilia B, less commom, caused by reduction in clotting factor IX.

These disorders are sex-linked, occurring only in males.

Laboratory evaluation includes a bleeding time, platelet count, partial thromboplastin time,
assay of factor VIII coagulant activity, von Willebrands factor antigen.

Replacement therapy with cryo-precipitate and possibly platelets, sufficient to normalize

bleeding time and factor VIII coagulant activity, is recommended for 7 days after surgical
procedures.

Acquired disorders: including;

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Drug-mediated thrombocytopenia.

Vitamin K deficiency: Vitamin K is essential for the synthesis of prothrombin and factors
VII, IX, and X. Vitamin K deficiency as a result of diet, disease, or medications.

Blood malignancies.

Liver disease: causes reduced levels of all coagulation factors except factor VIII.

Renal disease.

Vascular disorders:

Hereditary hemorrhagic telangiectasia (Osler-Rendu-Weber disease):

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Autosomal dominant inherited condition.

Telangiectasias have thin fragile vessel walls lined by a single endothelial layer with absent
smooth muscle, resulting in vessel fragility and impaired vasoconstriction.

Affects vessels from capillaries to large arteries.

In the nose, these lesions form raised lesions on the nasal septum, lateral nasal wall, and floor of
the nose. Their increased fragility may result in spontaneous epistaxis. Removal of crusts or
blood clots or excessive nose blowing will usually result in an epistaxis.

Arterio-venous malformations can be found in the brain, lungs, liver, and gut.

As these patients get older, regular nasal cautery will often result in the development of a septal
perforation.

Arteriosclerotic vascular disease:

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Arteriosclerotic vascular disease is a possible explanation for the higher incidence of nosebleeds
seen in those of increased age.

Although hypertension often is noted in the older patient with epistaxis, and although an
increased blood pressure reading is noted in the acutely bleeding patient, an actual increase in
frequency or severity of epistaxis in the hypertensive group has not been shown.

Management:
Observation
Antiseptic creams - Barrier ointments
Cauterization
Nasal packing: anterior pack, posterior nasal pack, nasopharyngeal balloon
Pterygopalatine fossa block
Laser photocoagulation
Pharmacologic control
Surgical
Arterial ligation
Angiographic embolization
Surgical reconstruction

Minor Hemorrhage:

Antiseptic creams are thought to work by reducing vestibulitis and mucosal inflammation as well as
by moistening the mucosa and preventing drying and crusting.

Barrier ointments are thought to work by preventing crusting of the septal mucosa.

Silver nitrate cautery may be used if, on examination of Little's area, a large dilated blood vessel is
seen that is thought to be the likely cause of the recurrent epistaxis.

Education about stopping crust removal and correct positioning of nasal sprays may reduce the
incidence of minor epistaxis.

Packs can be placed in the anterior nasal cavity. The pack is then removed after 20 minutes.

Major Hemorrhage:
Post-traumatic bleeding:

Anterior skull base fractures may cause damage to the anterior and posterior ethmoidal arteries,
whereas fractures of the maxilla may result in hemorrhage from the internal maxillary artery or one
of its branches. If the sphenoid is involved with fractures traversing the internal carotid artery,
catastrophic bleeding may result.

Ensure adequate intravenous access and Assessment and resuscitation of all vital signs in the
emergency room.

In cooperative patient:
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Patient is given a bowl and paper towels and told to blow all the blood clots out of his or her
nose.

Nasal cavity thoroughly sprayed with a combination of lidocaine, epinephrine (or adrenalin),
and saline.

Rigid nasal endoscope and suction are used to clear the nasal cavity of any residual blood clots
and attempts to identify site of bleeding, management accordingly.

In case of posterior packing; patients are admitted and should be monitored with pulse oximetry
because occlusion of the nasal cavity may induce hypoxia from activation of the nasopulmonary reflex and the consequent vascular shunting that occurs. In at-risk patients such
ischemia may be sufficient to trigger cardiac arrhythmias.

In comatosed patient:

Postnasal space balloon catheter is inserted into the nasopharynx and inflated with 15 mL
saline. In cadaveric studies, this volume has been shown to adequately occlude the postnasal
cavity and allow a platform onto which the ribbon gauze can be tightly packed.

Should bleeding continue, the patient should be taken to the operating room and endoscopic
examination of the nose performed under general anesthetic.

Bleeding from the region of the sphenopalatine artery can be managed by a sphenopalatine
artery ligation. If this fails to control bleeding, then the external carotid artery should be ligated
in the neck.

Bleeding from the roof of the nose can be managed endoscopically, or by a Lynch incision and
ligation of the anterior ethmoidal artery and the posterior ethmoidal artery if necessary.

Massive hemorrhage from the sphenoid region usually indicates an internal carotid injury.

Control of ethmoidal arteries:

Endoscopic:

Via a Lynch incision:

Recently, Douglas (Combined) approach: a limited (1-cm) incision is continued onto bone after
which a 4-mm endoscope is placed in the incision and dissection is continued in a subperiosteal
plane, anterior lacrimal crest identified, upper part of the lacrimal sac is lifted from the lacrimal
fossa and reflected laterally. Dissection continues posteriorly along the lamina papyracea following
the fronto-ethmoidal suture, artery is either clipped or cauterized.

+ Management of orbital hematoma.

Endoscopic Sphenopalatine Artery Ligation:

The procedure of choice for uncontrolled posterior epistaxis.

If the patient is actively bleeding, a pterygo-palatine block can be done by injectiong of 2 mL of

2% lidocaine and 1:100,000 adrenalin through the greater palatine canal (( landmarks for the
greater palatine canal are the point midway between the second molar tooth and the midline of the
palate. To locate the foramen of the greater palatine canal, it is often easier to place the endoscope
in the mouth and then to palpate the posterior edge of the palate sliding the finger forward until the
indentation of the foramen is felt. The endoscope is used to define this point and the finger is
withdrawn. Bent needle to about 15 mm (the length of greater palatine canal) is introduced
alongside the endoscope and into the depression identified. Injection of local anesthetic and

adrenalin causes vasospasm of the maxillary artery and will in most cases reduce or stop the
bleeding from the sphenopalatine artery or one of its branches. This allows the surgeon to be able to
operate in the nose without ongoing significant hemorrhage.

The first step is to palpate the posterior fontanelle of the maxillary sinus behind the uncinate
process. This region of the posterior fontanelle is soft.

Moving posteriorly, the hard bone of the palatine bone is felt.

At the junction of the posterior fontanelle and palatine bone, a vertical U-shaped incision is made
from under the horizontal portion of the middle turbinate.

Suction elevator is used to elevate the mucosa off the underlying bone until the anterior face of the
sphenoid is reached.

SPA is identified as it emerges from the sphenopalatine foramen. There is a bony prominence just
anterior to the sphenopalatine foramen (ethmoidal protuberance of the palatine bone) which can
be used as a landmark. This can be removed with a curette to further expose the sphenopalatine
foramen.

The artery must be dissected free from the other structures and tissue that emerges with it from the
palatine foramen until it is clearly seen as a single vessel.

Once this vessel has been clipped, further dissection posteriorly should be performed because the
posterior nasal artery that supplies the posterior aspect of the septum often divides prior to the
SPA emerging through the foramen and can be seen as a separate vessel posterior to the SPA; it
should be clipped as well.

Mucosal flap is then replaced and if necessary dissolvable packing is placed over the flap.

SPA ligation is successful in controlling epistaxis in 90% to 100% of patients.

Arteriography &
Embolization (Interventional radiology) of the Maxillary Artery:

This procedure is reserved as the 2nd choice for the small group of patients who continue to bleed
after SPA.

Can be useful for patients who are medically unfit to undergo SPA ligation.

It requires an interventional radiologist with significant experience and skill because the potential
complications from embolization are more serious than for arterial ligation.

Control rates for epistaxis vary from 65% to 85%.

Complications varying from stroke to facial pain and facial numbness.

Transantral Ligation of the Maxillary Artery:

Until recently, this was the procedure of choice, but it is rarely used today because SPA is easier,
has less complications, and is more effective at controlling epistaxis.

This procedure is performed by exposing the anterior face of the maxillary sinus and opening this
face in the same manner as would be done for the traditional Caldwell-Luc procedure. Once the
window is sufficient, the microscope is swung into place and the posterior wall of the maxillary
sinus is fractured and flaked off exposing the fat of the pterygopalatine fossa. The fat is teased out
and the blood vessels are identified.

The course of the maxillary artery through the pterygopalatine fossa is very tortuous, and it can be
difficult to identify whether the vessels exposed in this manner are the main trunk of the artery or
one of the branches. Thus it is relatively easy to miss either the main trunk of the artery or the
sphenopalatine branch, and this results in a failure rate of 10 to 20%.

Complications include facial paresthesia, facial pain, dental pain and numbness, hematoma, and
very rarely ophthalmoplegia and blindness.

Management of Hereditary Hemorrhagic Telangiectasia:

Laser Management:
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Lasers that are currently used are KTP, Nd:-YAG, and more recently pulse dye laser, because
they are selectively absorbed by the underlying microvasculature and coagulate the vessel with
a minimal damage to the surface epithelium.

One of the critical issues with laser treatment is the need to meticulously address all the
telangiectasias within the nose. This may take a number of hours; consequently, it is usually
performed under general anesthesia.

If there is an associated septal perforation, silastic septal splints are placed over the perforation
and held in place with a transseptal suture for 1 to 2 weeks before they are removed. This
allows the mucosa around the septal perforation to heal without crusting from turbulent airflow.

This needs to be repeated every 4 to 6 months as the patients grows new telangiectasias.

Septo-dermoplasty:
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Mucosa is removed, and kin grafts are placed on the nasal septum.

Although it is effective in the initial stages, over time the skin graft contracts and telangiectasias
are found at the junction of the graft and the mucosa.

Topically applied, OR Systemic Tranexamic acid (Cyclokapron):

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Antifibrinolytic that competitively inhibits the activation of plasminogen to plasmin, a molecule

responsible for the degradation of fibrin.

Recently described for patients with severe HHT.

Resulted in a significant reduction in bleeds per month.

Larger studies are necessary before this can be routinely adopted as part of the treatment for
HHT patients.

Management of ICA bleeding:

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If the patient is under general anesthetic, the blood pressure should be lowered by the
anesthetist to allow greater visibility for the surgeon and to facilitate the placing of packing
against the anterior face of the sphenoid sinus.

If possible, a sphenoidotomy can be performed and packing placed into the sphenoid to gain
control of the hemorrhage.

Muscle plug is harvested from the sternomastoid muscle in the neck. This muscle is placed
against the carotid artery in the sphenoid and a pack placed on top.

If this fails to control the hemorrhage, a temporary vascular clamp can be placed across the
common carotid artery in the neck while a sphenoidotomy is performed and the muscle and
pack placed in the sphenoid on the carotid artery. This clamp should be removed as soon as
possible to limit cerebral ischemia and the possibility of a stroke.

Patient is then sent for interventional arteriography. If the lesion is in the vertical portion of the
carotid in the sphenoid, then a stent may be placed, but if it is in the region of the carotid
siphon, then balloon occlusion of the carotid may be necessary and embolization of the
internal carotid may be the only solution for saving the patient's life. The major risk of carotid
occlusion is cerebral ischemia, hemiplegia, and, in some cases, death.

If the patient has undergone significant blood transfusions, then diffuse intravascular
coagulation may result in poor clotting and contribute to ongoing hemorrhage.