THE MANAGEMENT OF EPISTAXIS

Epistaxis can be defined as bleeding emanating from the internal nose. Epistaxis is
a frightening experience for the patient. Most cases are easily controlled and can be
managed on an outpatient basis. On the other hand, epistaxis can be a life-threatening
problem. It is important that the clinician has a logical approach to the management of
epistaxis. Management will include the establishment of haemostasis, identification and
treatment of hypovolaemia or circulatory shock (when present) and the specific
management of any aetiologic factor.

BLOOD SUPPLY OF THE INTERNAL NOSE

The nose is supplied by both the external carotid and internal carotid arterial
systems and there are multiple anastomoses between these systems in the nose.
The major blood supply is via the maxillary branch of the external carotid artery.
Venous drainage
The venous drainage of the central parts of the lateral nasal wall is to the pterygoid
venous plexus. The anterior areas drain to the facial vein while posteriorly the drainage is
to the pharyngeal venous plexus.
The specific blood supply to the septum must be reviewed, as this is the commonest
source of epistaxis.

The blood supply of the nasal septum

The major source of arterial blood to the nasal septum is the sphenopalatine branch of the
maxillary artery. The ascending branch of the greater palatine artery passes through the
incisive canal to anastomose with the sphenopalatine, the superior labial and the anterior
ethmoidal arteries at Little's area on the antero-inferior portion of the septum. The plexus
of arteries at this site is called Kiesselbach's plexus. The commonest site for epistaxis is
Little's area. The posterior ethmoidal artery gives a small contribution to the antero-
superior aspect of the septum.
Venous drainage
The septum drains anteriorly to the facial vein, posteriorly to the pterygoid venous plexus
and superiorly via ethmoidal veins to the ophthalmic veins. In 1% of individuals, the
nasal veins are connected to the superior sagittal sinus by a vein that passes through the
foramen caecum in front of the crista galli. The retrocumellar vein is an important source
of venous bleeding in children and young adults.

There are important anastomoses across the midline between the two anterior
ethmoidal vessels and also occurring in the nasopharynx. This can explain some of the
cases in which arterial ligation fails to control epistaxis.

Causes of epistaxis
Examples of local causes
a) Trauma: trivial or major injuries, nasal fracture, surgical trauma, foreign body,
excessive sneezing or coughing (with increased pressure in the nasal vessels).
b) Inflammation, infection and allergy: e.g. acute and chronic, specific and non-specific
rhinitis.
c) Neoplasms (and tumour- like masses) of the nose, nasopharynx and sinuses:
1) Benign - angiofibroma, haemangioma, inverted papilloma, pyogenic granuloma
(tumour-like), other granulomas.
2) Malignant - squamous cell carcinoma, adenocarcinoma, salivary gland tumours,
melanocarcinoma, midline lethal granuloma (generally considered a lymphoma).
d) Drugs - cocaine abuse.
c) Congenital vascular malformation.

In many cases of epistaxis the actual aetiology is never elucidated. These cases are
often labelled as spontaneous epistaxis but a careful clinical assessment will often
reveal contributory factors such as minor trauma and inflammation.
Examples of general causes
Abnormal bleeding may result from a defective coagulation pathway,
thrombocytopaenia, platelet function defects and vascular abnormalities.
A) Congenital coagulopathies e.g. haemophilia, Christmas disease, von Willebrand's
disease.
B) Acquired defects in the coagulation pathway: heparin or warfarin therapy; hepatic or
obstructive biliary diseases.
C ) Thrombocytopaenia
1) Platelet production failure
i) Selective depression of the megakaryocytes by drug toxicity (cotrimoxazole,
phenylbutazone, thiazides, tolbutamide) or viral infections.
ii) Generalised bone marrow failure: plastic anaemia, leukaemia, marrow
infiltration or myelosclerosis.
iii) Ineffective platelet production: megaloblastic anaemia.
2) Increased platelet destruction:
i) Idiopathic thrombocytopaenic purpura
ii) Secondary immune thrombocytopaenia ( post-infection, SLE, chronic
lymphocytic leukaemia) iii) Disseminated intravascular coagulation
iv) Drug- induced immune thrombocytopaenia (sulphonamides, quinine, PAS,
rifampicin digitoxin).
3) Splenic pooling in patients with splenomegaly.
4) Massive transfusion of old blood: dilutional thrombocytopaenia
D) Abnormal platelet function
Aspirin therapy, hepatic and renal disease, multiple myeloma and Waldenstrom's
macroglobulinaemia are all acquired causes of platelet dysfunction .
E) Vascular abnormalities: Hereditary haemorrhagic telangiectasia, steroid-induced
vascular weakness, scurvy, Monckeberg's sclerosis.
Hypertension and anxiety tend to cause prolongation of epistaxis but the incidence
 of epistaxis is not increased in these patients. Hypertension is associated with
vascular changes, which inhibit vasoconstriction thus prolonging epistaxis. The
increased arterial pressure will also increase the severity of the epistaxis. Thus
hypertensive patients are more frequently admitted to hospital for the control of
epistaxis. The control of hypertension is an essential part of the management of
epistaxis in the hypertensive patient.

Management of active epistaxis

History
A brief history is obtained from the patient or a relative while preparations are
being made to control the epistaxis. It is useful to inquire whether the epistaxis is
predominantly an anterior or posterior bleed and whether the epistaxis is unilateral. If the
bleeding is reported as bilateral, one should still inquire as to the side that initially bled
(often blood is entering the opposite nasal passage at the posterior choanae by passing
around the border of the septum). It is important to ask about any syncopal sensation,
which may be indicative of cardiovascular decompensation. The patient should be asked
to give an estimate of the blood loss in terms of common utensils such as cups or
tablespoonfuls. Patients tend to exaggerate the blood loss, but often have containers with
them that they have used to collect the blood and these can be very helpful in estimating
the blood loss. One should ask about nasal trauma( including nose-picking), upper
respiratory tract infections, recent medications, history of bleeding diathesis and any
significant medical illness.
It should be clear that the thoroughness of the initial history would depend on the
clinical status of the patient. The patient who is in hypovolaemic shock will require
emergency resuscitation while attempts are made to control the bleeding. The patient
whose cardiovascular system is stable but who is bleeding heavily is best managed by
controlling the bleeding and then completing the history.
Examination
The patient's pulse and blood pressure should be taken. If the cardiovascular
system is stable the patient should be examined sitting up or in the semi-recumbent
position. Strong suction and a good headlight are prerequisites for an adequate
assessment of the patient with epistaxis. It is useful to attempt a preliminary assessment
of the nose without vasoconstriction because this can sometimes stop the bleeding and
prevent identification of the bleeding point. After suctioning the clots, local anaesthetic
and vasoconstrictive nasal drops or sprays will facilitate examination of the nose and
assist with haemostasis in patients who are not bleeding profusely. Cocaine is a very
potent vasoconstrictor and local anaesthetic and is therefore frequently used in this
setting. The maximum dose should be 1.5mg/kg. An alternative preparation is a mixture
of 0.1% xylometazoline and lignocaine.
While local measures are being undertaken, it is important that resuscitation of the
circulatory volume with intravenous fluid and blood transfusion (if necessary) is carried
out. Sedation should be prescribed as this relieves the patient's anxiety, reduces the blood
pressure and facilitates nasal cautery and packing.
Anterior epistaxis
Effective treatment for anterior epistaxis includes tamponade of the nasal vessels
between the fingers, nasal cautery, nasal packing, and surgery with ligation of the
anterior ethmoidal artery. Most patients who are being assessed by an otolaryngologist
will have already attempted to tamponade the nasal vessels between the fingers, but may
not have applied pressure properly and so the otolaryngologist should give the relevant
instructions. The patient can attempt to tamponade the nasal vessels while preparations
are being made to examine the nose.
If the source of an anterior epistaxis is identified, the treatment of choice is nasal
cautery. This treatment is usually successful unless the bleeding is profuse. The
commonest site of epistaxis is Little's area on the antero-inferior nasal septum. The
immediate area around the focus of bleeding should first be cauterised before cautery to
the actual bleeding site is attempted, otherwise there would be a significant risk of
aggravating the epistaxis. Successful nasal cautery has the advantage of avoiding nasal
packs. Patients who have not had major bleeds with cardiovascular decompensation can
often go home after a short period of 20- 30 minutes of observation for recurrent
bleeding. Silver nitrate, trichloro-acetic acid and electrocautery are highly effective.
Electrocautery is the more effective than chemical cautery in the presence of active
bleeding, but would require general anaesthesia in children
There is a risk of septal perforation when unilateral cautery is overzealously performed.
Bilateral nasal cautery at equivalent sites on the nasal septum should be avoided, as this is
associated with a high incidence of perforations.
Nasal packs will be required in cases of profuse anterior epistaxis and in cases
where the focal bleeding point cannot be identified. A half- inch petrolatum gauze-strip
soaked in antibiotic ointment or bismuth iodoform paraffin paste (BIPP) packing is
commonly used. The nasal packing should be applied meticulously, in loops, from the
nasal floor to the nasal roof and extending as far posteriorly as is feasible. Patients often
find the insertion and the removal of these packs very uncomfortable. Adequate local
anaesthesia and analgesia should be administered. Merocel sponges can be inserted easily
and are better tolerated. These are especially useful in children. Experience with Merocel
sponges suggest that they are less effective than BIPP or gauze strip packs. They are most
useful in mild epistaxis. Gauze strip packs, BIPP and Merocel all adhere to the nasal
mucosa to varying degrees and epistaxis may resume on removal of the nasal packs.
Nasal balloons are easy to insert and to remove, but are slightly less effective than
traditional nasal packs in controlling epistaxis because they do not adapt very well to the
irregularity of the lateral nasal wall.
Anterior nasal packs should be left in situ for 24-48 hours. During this period the
patient should be on antibiotics and should be nursed propped up so that that the
head is elevated.
.
Nasal endoscopy
Nasal endoscopy has increased the frequency with which the actual bleeding point
is identified. This has facilitated both chemical and electro-cautery. Nasal endoscopy has
been particularly helpful in epistaxis that is relatively posterior in location. The 0 and the
30 degrees rigid telescopes or the flexible fibreoptic scopes can be used. The flexible
fibreoptic scope is particularly useful in identifying bleeding points that are posterior to
septal deviations.
Occasionally septoplasty(operation to straighten the septum) must be performed to
facilitate access to a bleeding point so that cautery or effective nasal packing can
be accomplished.

Treatment options for posterior epistaxis

Posterior epistaxis can be very difficult to manage. Identification of the bleeding
point is sometimes impossible and one has to rely on post- nasal packs or balloon
tamponade initially if significant active bleeding is occurring. Sometimes the patient
presents with mild posterior epistaxis. In these cases the nose should be decongested and
topical anaesthesia applied to facilitate examination endoscopically or microscopically. It
is worthwhile to attempt a preliminary nasal examination without the use of
vasoconstriction as the latter occasionally stops the bleeding and prevents identification
of the bleeding point. If the bleeding point is identified, the site should be cauterised. In
cases where heavy posterior bleeding is occurring, the initial management should be the
insertion of a double-lumen balloon to apply nasal as well as postnasal tamponade since
one would not be certain of the exact source of the bleeding. This method also increases
the efficiency of the tamponade. Under local anaesthesia, nasal balloons can be inserted
quickly and easily with minimal discomfort to the patient. Nasal balloons are tolerated
much well than the traditional anterior and posterior nasal packs. The nasal balloons
should remain in situ for 48 - 72 hrs.
If bleeding persists despite the insertion, or on the removal, of the nasal balloons,
endosopic or microscopic examination of the nose should be performed. If the epistaxis is
not controlled by posterior endoscopic microscopic cautery, then a Foley's catheter
should be inserted and the balloon inflated with 15 ml of air or saline. Saline does carry
with it the tiny theoretical risk of aspiration but has the advantage that it does not leak as
easily as air. Bilateral anterior nasal packs (petrolatum gauze strips) should also be
inserted to maximise the tamponade effect.
When posterior endoscopic cautery (under local anaesthesia) and nasal packs fail
to control epistaxis, or epistaxis recurs on removal of the packs, the nasal passages and
the postnasal space should be examined under general anaesthesia. Any bleeding point
that is identified should be cauterised. Identification of the bleeding point may require
fracturing the turbinates to allow access to the meati. If the bleeding site cannot be
identified, the maxillary artery should be ligated. The alternative is to insert firm anterior
and posterior nasal packs under general anaesthesia, leave these in situ for 72- 96 hrs and
to proceed to ligate the maxillary artery if bleeding recurs on removal of the packs. It is
perhaps a better choice to avoid two general anaesthesias and to proceed with ligation of
the maxillary artery at the first general anaesthesia.
Ligation of the maxillary artery is effective in 95% of cases. Embolization of the
maxillary artery using gelfoam, has been successful in controlling epistaxis, but has a
higher failure rate than ligation of the maxillary artery and its sphenopalatine and greater
palatine branches. It is rarely necessary to ligate the anterior ethmoidal vessels when
adequate ligation of the maxillary arteries and its main branches has been performed.

Special conditions
There are many possible causes for epistaxis. In the management of epistaxis one
should be careful not to miss a malignancy of the nose, sinuses or the nasopharynx.
Careful clinical assessment and radiologic studies will identify these malignancies. The
male teenager may have an angiofibroma requiring angiography and CT scanning to
plan the surgical approach to be utilised after embolization of the major feeding vessels.
Patients who have hereditary haemorrhagic telangiectasia are difficult to manage.
Septodermoplasty has produced transient success but telangiectactic vessels tend to
grow into the split skin graft with resultant recurrent epistaxis. Oestrogens and local
radiotherapy have been useful in some cases. Recurrent bleeding from the edges of a
septal perforation can be controlled with cautery.
 MANAGEMENT OF SINUSITIS
Acute sinusitis is defined as an acute inflammation of the paranasal sinuses, which
resolves without residual mucosal change following appropriate medical therapy.
Children who meet the following criteria are categorised as having chronic sinusitis:
a) Persistent symptoms and signs for twelve weeks
or six episodes per year of recurrent acute sinusitis
b) in association with persistent mucosal change on CT scan four weeks after
medical therapy
(International Conference on Sinus Disease: terminology, staging, therapy ---
- 1993)
The paranasal sinuses develop as outgrowths from the lateral wall of the nose
starting at the 40th gestational day. At birth, only the maxillary and the ethmoidal sinuses
are readily identifiable. Most of the subsequent growth of the maxillary sinus depends on
the eruption of the dentition. The frontal sinus usually develops from anterior ethmoidal
air cells called the frontal recess. The majority of the paranasal sinuses drain into the
middle meatus. Normal physiology of the paranasal sinuses depends on the patency of the
ostia of the sinuses, good mucociliary function and adequate immune function.
Sinusitis is often initiated by obstruction of the ostiomeatal complex, which results
in hypoxia of the sinus mucosa and ciliary dysfunction. This produces stasis of the
sinonasal secretions and multiplication of bacteria. The inflammatory response
perpetuates the obstruction of the ostia. Thus patients may have a primary lesion
obstructing the ostia or inflammation may produce secondary obstruction of the ostia.
Chronic sinusitis develops if the obstruction is not relieved. Persistent disease in the
sinuses is usually secondary to disease in the anterior ethmoids and the ostiomeatal
complex (middle meatus and adjoining areas). Medical and surgical management must
attempt to correct the abnormalities in these key areas.
A thorough history and a full examination are essential in each patient. However it
is often difficult to examine the middle meatus without the use of nasal endoscopes.
When the middle meatus is not seen and symptoms and signs of purulent rhinorrhoea,
postnasal discharge and nasal obstruction persist for more than ten days a presumptive
diagnosis of rhinosinusitis should be made. It is also reasonable to make a diagnosis of
rhinosinusitis in the patient who has nasal symptoms associated with pain in the region of
the sinuses.
In the past we relied heavily on plain X-rays in the investigation of the sinuses.
Mucosal thickening, sinus opacification and fluid levels are often indicative of sinusitis.
It is now possible to assess the sinuses with great precision. The state of the art
techniques in the assessment of the sinuses are nasal endoscopy and high resolution
computerised tomography. Nasal endoscopy has allowed us to examine areas that were
previously inaccessible without general anaesthesia. Patients with suspected
complications of sinus disease (e.g. orbital and intracranial complications) and those
with persistent symptoms and signs despite adequate medical therapy require
computerised tomography. This will allow precise planning of the surgical approach in
each patient.

Complications of Sinusitis

Local
1. Chronicity and irreversible mucosal change
2. Mucocele
3. Osteomyelitis especially of the diploic anterior wall of frontal sinus

Orbital complications

(1) Dacrocystitis because of obstruction of the Naso-Lacrimal Duct.

(2) Conjunctivitis
(3) Subperiosteal abscess
(4) Periorbital cellulitis
(5) Orbital Cellulitis
(6) Orbital abscess
(7) Ophthalmoplegia
(8) Blindness

Intracranial Spread
Epidural Abscess
Meningitis
Subdural Abscess
Frontal lobe Abscess
Cavernous sinus thrombosis

Note that the paranasal sinuses are the commonest source of frontal lobe abscess.

Medical therapy of Sinusitis aims to control infection, establish patency of the ostia,
relieve symptoms and treat predisposing conditions. Streptococcus pneumoniae and
Haemophilus influenzae are responsible for 76% of cases of community-acquired
sinusitis. Anaerobes, other streptococcal species, Moraxella catarrhalis and
Staphylococcus aureus each account for 3-7% of cases. Amoxicillin plus Clauvulanic
acid, and Cefuroxime are considered as good first line antibiotics.