EPISTAXIS

BY DR. EYRAM ETSEY

OUTLINE
 Introduction
 Vascular Anatomy
 Classification
 Types of Epistaxis
 Etiology
 Pathophysiology
 Clinical Presentation
 Investigation
 Complications
 Management
INTRODUCTION
• The term “Epistaxis” came from the Greek word
“epistazein” which means “bleed from the nose’.

• Epistaxis, or nasal bleeding, is defined as an

acute hemorrhage originating from the nostrils,
nasal cavity, or nasopharynx.

• Epistaxis is a common condition encountered in

clinical practice and, while often benign, it can
occasionally present as a life-threatening
emergency, especially when bleeding is profuse
or uncontrolled. The bleeding may be unilateral
or bilateral.
Vascular Anatomy
The nasal mucosa is richly vascularized,
primarily by branches from both the internal
and external carotid arteries.

• External Carotid artery

Sphenopalatine artery of maxilliary artery
Greater palatine artery
Superior labial artery of facial artery

• Internal carotid artery

Anterior ethmoidal artery
Posterior ethmoidal artery

The nasal cavity is mostly supplied by the

sphenopalatine artery.
Vascular Anatomy
• The two main plexuses involved in epistaxis are:
 Kiesselbach’s plexus (Little’s area) – located on the anterior part of the nasal septum, it is
the most common site of bleeding (about 90% of cases). It represents a confluence of:
• * Anterior ethmoidal artery (ophthalmic branch, internal carotid)
• * Sphenopalatine artery (maxillary branch, external carotid)
• * Greater palatine artery
• * Superior labial artery (facial artery)
 Woodruff’s plexus – located in the posterior nasal cavity, and is made up of anastomosis
between branches of the internal maxilliary artery namely sphenopalatine artery and
ascending pharyngeal artery. It accounts for more severe posterior epistaxis.
 These plexuses are vulnerable to trauma, drying, inflammation, or systemic vascular insults.
Vascular anatomy
CLASSIFICATION

Anterior Epistaxis Posterior Epistaxis

Blood flows out from front of Blood flows back into the
the nose throat.
CLASSIFICATION
Anterior Epistaxis Posterior Epistaxis
Incidence More common Less common
Site Mostly from Little’s area or anterior part Mostly from posterior part of nasal cavity
of lateral wall
Age mostly occurs in children or young adults After 40 years of age
Cause Mostly trauma or by nasal mucosa Spontaneous; often due to hypertension or
dryness arterosclerosis

Bleeding Usually mild and can be controlled by Bleeding is severe and requires
local pressure or anterior pack hospitilization; postnatal pack often used
TYPES OF EPISTAXIS
 Recurrent Epistaxis is characterized by repeated episodes of nasal bleeding that occur
intermittently over time, often following a seasonal pattern. Notably, these episodes
frequently coincide with periods of hot, dry weather, which promote nasal mucosal
desiccation and crust formation, thereby increasing vascular fragility and the risk of
spontaneous hemorrhage.
 Constant epistaxis refers to a prolonged, continuous episode of nasal bleeding, typically
lasting 30–45 minutes or more, without spontaneous resolution.
 Sudden epistaxis describes an abrupt onset of nasal bleeding that may occur at any time of
day, irrespective of the individual’s activity level—be it at rest or during physical exertion.
 Chronic epistaxis is defined as persistent or frequently recurring nasal bleeding lasting
more than six months, often secondary to an underlying chronic condition.
ETIOLOGY
A. Idiopathic (primary)
B. Local Causes
i. Congenital (Hereditary Hemorrhagic Telangiectasia- Osler Weber- Rendu syndrome)
ii. Trauma
• Microtrauma (nose picking)
• Accidental (facial injury)
• Iatrogenic (nasal instrumentation eg nasogastric tube)
• Barotrauma (Caisson’s disease - decompression sickness)
iii. Infections
• Viral : Influenza, common cold, measles
• Bacterial: nonspecific (rhinitis, sinusitis)
specific (nasal diphtheria , TB, syphilis)
ETIOLOGY
• Fungal : rhinosporidiosis, fungal sinusitis
• Parasites: maggots
iv. Physiological causes
• High altitudes
• Extreme cold/ hot climate
v. Neoplasia( Bening: Capilliary and Cavernous hemangioma, Inverted papilloma, angioma of
septum. Malignant: Nasopaharyngeal carcinoma, olfactory neuroblastoma and Squamous
cell carcinoma)
vi. Miscellaneous
• Deviated nasal septum, spur (causes crusting eddy air currents, dryness of nasal mucosa
and crusting)
• Rhinolith
ETIOLOGY
C. General causes
i. Cardiovascular
• Hypertension, arteriosclerosis, Mitrial stenosis
ii. Liver Cirrhosis (ViT K deficiency, Deficiency of factor II,VII,IX and X)
iii. Kidney disease (Chronic nephritis)
iv. Hematological (Aplastic anemia, Von Willebrand disease,Thrombocytopenia, leukemia,
Lymphoma, Agranulocytosis,
Scurvy)
v. Drugs ( Excessive use of salicylates and other analgesics. anticoagulant therapy.
Topical nasal steroids or decongestants.)
vi. Vicarious Menstruation.
PATHOPHYSIOLOGY
Epistaxis typically follows a multi‑step sequence involving both local vascular injury and
systemic modulation:
1. Vascular Vulnerability or Initiating Trigger
Fragile nasal mucosal vessels—particularly in Kiesselbach’s plexus—are predisposed to injury
from mechanical trauma (e.g. nose-picking, nasal cannula use), inflammatory insults (rhinitis,
dry crusting), or underlying systemic disease such as hypertension, arteriosclerosis, or vascular
malformations (e.g. HHT)
2. Vessel Rupture (Capillary or Arterial)
Minor trauma or mucosal thinning can rupture small capillaries or venules (anterior bleeds),
whereas deeper arterial vessels such as branches of the sphenopalatine artery or Woodruff’s
plexus may rupture in posterior bleeds—often resulting in high-pressure, brisk hemorrhage
3. Ineffective Vasoconstriction or Clot Formation
The body’s immediate hemostatic response—vasoconstriction, platelet plug formation, and
fibrin stabilization—is often sufficient for minor anterior bleeds. However, coagulopathies,
anticoagulant use, or vascular disease can impair these mechanisms, preventing effective clot
formation and allowing bleeding to persist
 PATHOPHYSIOLOGY
4. Persistent Bleeding, Sometimes with Posterior Drainage
When initial control fails, bleeding continues—anteriorly visible or, in deeper bleeds, draining
into the oropharynx or swallowed. Posterior drainage may obscure source localization and
contribute to risk of aspiration or hemodynamic compromise
5. Systemic Factors That Worsen Severity or Delay Resolution
Patients with hypertension, cardiovascular or peripheral vascular disease, chronic liver disease,
or hematologic malignancies are more likely to experience severe or refractory epistaxis. These
conditions impair vessel resilience and clotting ability, prolong bleeding, and increase
recurrence risk
 CLINICAL PRESENTATION
Anterior Posterior
• Bleeding usually unilateral Slow • Characterized by heavier, brisk
bleeding, often bilateral or with
to moderate oozing, often visible
blood draining into the oropharynx
on anterior rhinoscopy
• Patients may experience nausea,
• Patients may report crusting, vomiting, or hematemesis from
dryness, or recent nasal trauma swallowed blood
(e.g. nose-picking, forceful
blowing) • May present with dizziness,
weakness, hypotension, or
• Systemic signs usually absent tachycardia if significant blood
unless bleeding is prolonged loss has occurred
INVESTIGATIONS
 Laboratory Investigations
• Full Blood Count
• Clotting profile
• Blood grouping and crossmatching
• Liver function test
• Renal function test etc.
 Imaging studies
• X-ray paranasal sinuses
• CT scan, MRI
• Digital subtraction angiography- useful in identifying bleeding vessels in profuse or recurrent
epistaxis
 Other procedures
• Rhinoscopy (anterior and posterior)
• Endoscopy
COMPLICATIONS
• Anemia & Hypovolemic Shock
Severe or persistent bleeding—especially from posterior sources—can lead to significant blood
loss, resulting in anemia or even hypovolemic shock in predisposed patients
• Aspiration of Blood
Blood may be inadvertently inhaled into the airway, particularly during posterior epistaxis or in
immobilized patients, risking respiratory distress or pneumonia
• Sinusitis
Secondary infection of the paranasal sinuses may develop after bleeding or clot formation
within the nasal cavities
• Septal Hematoma or Perforation
Unrecognized septal hematomas can develop, leading to cartilage necrosis and perforation if
untreated; can also progress to external nasal deformity such as saddle nose
• Vasovagal Episode
Fainting or bradycardia due to vagal stimulation during bleeding has been reported, especially
in anxious patients
MANAGEMENT
In any case of epistaxis, It is important to know
• Mode of onset
• Duration and frequency of bleeding
• Amount of blood loss
• Site of nose from where bleeding is occuring
• Bleeding type : anterior or posterior
• Any known bleeding tendency in patient/ family
• History of known medical ailment ( hypertension, leukaemia, mitral valve disease, cirrhosis,
nephritis)
• History of drug intake(analgesics, anticoagulant etc)
• NB: Most cases are self limiting and thereby do not require medical treatment
 MANAGEMENT
First aid / Manaul Hemostasis
• Compression of the nostil:Pinching the
nose with thumb and index finger for
aboiut 5-10mins. This compresses the
vessels of the Little’s area
• In Trotter’s method patient is made to
sit, leaning a little forward over a basin
to spit out blood that collects in
pharynx, and breathe quietly from the
mouth. (this stops active bleeding from
the septum)
• Cold compresses (ice cubes) to the
nose to cause reflex vasoconstriction
or application of cotton wool soaked
with vasoconstrictor ( epinephrine)
MANAGEMENT
Cauterization
• In anterior epistaxis when bleeding has
been located, chemical/electrocautery
may be done using 20% silver nitrate,
3% trichloroacetic acid
• Local anesthesia is given and the
bleeding point cauterized with a bead
of silver nitrate or coagulated with
electrocautery
• The effectiveness of both cauterization
methods can be enhanced by using
rigid endoscopy, especially in the case
of more posteriorly located bleeding
sites
MANAGEMENT
Anterior nasal packing
• If bleeding is profuse and/or the site of bleeding is difficullt to localise, anterior packing is
done
• Roller gauze soaked with liquid parrafin, vaseline or bismuth iodoform parrafin paste.
Instruments used are nasal speculum and Tiley’s nasal dressing forceps
• About 1m long gauze 92.5cm wide in adults and 12mm in children is required for each nasal
cavity. First , few centimetres of gauze are folded upon itself and inserted along the floor, and
then the whole nasalcavity is packed tightly by layering the gauze from floor to the roof
• It can be romoved after 24hrs if bleeding has stopped
• If it has to be kept for 2 to 3 days; systemic antibiotics should be given to prevent sinus
infection and toxic shock syndrome
• Alternatively Hemostatic agents like Gelatin sponge(Gelfoam), Merocel? surgicel may be
used.
MANAGEMENT
• Gelfoam provides tamponade to the site of bleeding, promotes clot formation with early sealing
of blood vessels and it is not to be removed as it gets absorbed.
MANAGEMENT
Ballon tamponade

Best suited in epistaxis due to bleeding or clotting disorder

 MANAGEMENT
Posterior nasal packing
• For patients bleeding posteriorly
into the throat.
• A postnasal pack is prepared
tying three silk ties to a piece of
gauze rolled into a shape of a
cone or cylinder which is
soaked in liquid paraffin.
• Patients requiring postnasal
pack should always be
hospitalised
• Folley’s cathether can be used
MANAGEMENT
• Ligation of vessels (External carotid, Maxilliary artery, Ethmoidal arteries
• Embolization: Bleeding from the External Carotid Artery system may be
controlled with embolization
REFRENCES
• https://emedicine.medscape.com/article/863220-overview
• https://www.slideshare.net/slideshow/epistaxis-14073487/14073487#8
• https://emedicine.medscape.com/article/863220-clinical#b3
• https://www.youtube.com/watch?v=z1PSIcqDQWI
• https://www.youtube.com/watch?v=Xw6p8VvltIE
• https://www.youtube.com/watch?v=KuOiUZ1p6F8&t=637s