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CSF Rhinorrhea


Cerebrospinal fluid (CSF) consists of a mixture of water, electrolytes (Na+, K+, Mg2+,
Ca2+, Cl-, and HCO3-), glucose (60-80% of blood glucose), amino acids, and various proteins
(22-38 mg/dL). CSF is colorless, clear, and typically devoid of cells such as
polymorphonuclear cells and mononuclear cells (< 5/L).

The primary site of CSF production is the choroid plexus, which is responsible for 50-80%
of its daily production. Other sites of production include the ependymal surface layer (up to
30%) and capillary ultrafiltration (up to 20%). CSF represents the end product of the
ultrafiltration of plasma across epithelial cells in the choroid plexus lining the ventricles of
the brain. A basal layer Na+/K+ ATPase is responsible for actively transporting Na+ into
epithelial cells, after which water follows across this gradient. Carbonic anhydrase catalyzes
the formation of bicarbonate inside the epithelial cell. Another Na+/K+ ATPase lining the
ventricular side of the epithelium extrudes Na+ into the ventricle, with water following across
this ionic gradient. The resulting fluid is termed cerebrospinal fluid.

CSF is produced at a rate of approximately 20 mL/h for a total of approximately 500 mL

daily. At any given time, approximately 90-150 mL of CSF is circulating throughout the
CNS. CSF produced at the choroid plexus typically circulates from the lateral ventricles to
the third ventricle via the aqueduct of Sylvius. From the third ventricle, the fluid circulates
into the forth ventricle and out into the subarachnoid space via the foramina of Magendie and
Luschka. After circulating through the subarachnoid space, CSF is reabsorbed via the
arachnoid villi.

Circulation of CSF is maintained by the hydrostatic differences between its rate of

production and its rate of absorption. Normal CSF pressure is approximately 10-15 mm Hg,
and elevated pressure constitutes an intracranial pressure (ICP) greater than 20 mm Hg.

CSF rhinorrhea is a rare but potentially devastating condition that can lead to significant
morbidity and mortality for the patient. Disruption of the barriers between the sinonasal
cavity and the anterior and middle cranial fossae is the underlying factor leading to the
discharge of CSF into the nasal cavity. The resulting communication with the CNS can result
in a multitude of infectious complications that impart significant morbidity and potentially
disastrous long-term deficits for the patient.

This article discusses current concepts in the etiology, diagnosis, and treatment of CSF
rhinorrhea, as well as long-term management of patients following successful treatment.

See the image below.

An axial CT of a patient with a spontaneous CSF leak reveals a defect in the posterior

table of the left frontal sinus.

History Of The Procedure

From the first intracranial repair in the 1900s to the use of endoscopes and image-
guidance systems, the management of cerebrospinal fluid (CSF) rhinorrhea has greatly
evolved. Dandy is credited with the first surgical repair of a CSF leak via a frontal
craniotomy approach in 1926. Various other authors, including Dohlman (1948), Hirsch
(1952), and Hallberg (1964), subsequently reported successful repair of CSF rhinorrhea
through different external approaches. In 1981, Wigand reported on the use of the endoscope
to assist with the repair of a skull base defect. Since then, endoscopic repair has become the
preferred method of addressing CSF rhinorrhea, given the high success rate of 90-95% and
the decreased morbidity associated with this approach.


The underlying defect responsible for cerebrospinal fluid (CSF) leaks, regardless of the
etiology, is the same: disruption in the arachnoid and dura mater coupled with an osseous
defect and a CSF pressure gradient that is continuously or intermittently greater than the
tensile strength of the disrupted tissue.


The frequency of cerebrospinal fluid (CSF) rhinorrhea is determined by the underlying

etiology. Please refer to Etiology for further details.


Cerebrospinal fluid (CSF) leaks are generally classified as traumatic, iatrogenic, and
spontaneous/idiopathic. Traumatic causes include both blunt and penetrating facial injuries.
Iatrogenic causes include neurosurgical and otolaryngologic approaches to neoplastic disease,
as well as functional endoscopic sinus surgery (FESS). Most spontaneous, or primary, causes
of CSF rhinorrhea are now thought actually to be secondary to elevations in intracranial
pressure (ICP) that might be seen in patients with idiopathic intracranial hypertension (IIH).
Congenital skull base defects and certain tumors can also lead to CSF rhinorrhea.

Traumatic CSF rhinorrhea

Penetrating and closed-head trauma are responsible for 90% of all cases of CSF leaks.
CSF rhinorrhea following a traumatic injury is classified as immediate (within 48 hours) or
delayed. The majority of patients with a CSF leak due to accidental trauma (eg, motor vehicle
accident) present immediately. Most of the patients (95%) with a delayed CSF leak present
within 3 months after the injury.

Iatrogenic CSF rhinorrhea

In contrast to traumatic leaks, only 50% of patients with iatrogenic CSF leaks present
within the first week after the insult. In most cases, the patient will have been discharged
when the leak presents itself. Hence, educating the patient regarding the common symptoms
associated with a CSF leak such as salty or metallic taste is of paramount importance.

Any surgical manipulation near the skull base can result in an iatrogenic CSF leak. Skull
base injuries can vary from simple cracks in the bony architecture to large (>1 cm) defects
with disruption of the dura and potentially brain parenchyma.
Otolaryngology procedures, including FESS and septoplasty, can lead to a skull base
defect and CSF rhinorrhea. Certain neurosurgical procedures such as craniotomy and
transsphenoidal pituitary resections are most commonly associated with an increased risk of
CSF rhinorrhea.

In patients undergoing endoscopic sinus surgery, the site of injury is most frequently the
lateral lamella of the cribriform plate, where the bone of the anterior skull base is thinnest.
Other common locations include the posterior fovea ethmoidalis and the posterior aspect of
the frontal recess.

Tumor-related CSF rhinorrhea

The growth of benign tumors does not commonly result in CSF rhinorrhea. However,
locally aggressive lesions such as inverted papilloma and malignant neoplasms can erode the
bone of the anterior cranial fossa. The enzymatic breakdown or destruction of the bony
architecture results in inflammation and potential violation of the dura. Even if the tumor
itself does not lead to CSF rhinorrhea, the resection typically results in immediate leakage.
Hence, the surgical team should be prepared to repair the resulting CSF leak at the time of the
resection, either transcranially or endoscopically.

Congenital CSF rhinorrhea

Defects in the closure of the anterior neuropore can result in the herniation of central
nervous tissue through anterior cranial fossa. These are infrequently associated with CSF
rhinorrhea. The embryologic defect is typically a patent fonticulus frontalis or foramen
cecum. Meningoencephaloceles usually present in childhood as an intranasal/extranasal mass
that transilluminates and expands with crying (Furstenberg sign). A high index of suspicion
should be maintained with all pediatric intranasal masses, particularly those occurring at the
midline. A biopsy should never be obtained unless a complete imaging workup has been

Spontaneous CSF rhinorrhea

Spontaneous CSF rhinorrhea occurs in patients without antecedent causes. This

terminology seems to imply that spontaneous CSF leaks are idiopathic in nature; however,
recent evidence has led us to realize that spontaneous CSF rhinorrhea may in reality be
secondary to an intracranial process, namely elevated intracranial pressure (ICP). There are
several causes of elevated ICP; however, the proposed mechanism underlying spontaneous
CSF rhinorrhea is idiopathic intracranial hypertension (IIH). Obstructive sleep apnea (OSA)
has also been linked to elevated ICP.

Despite the multifactorial causes of elevated ICP, once this problem ensues, the pressure
exerted on areas of the anterior skull base such as the lateral lamella of the cribriform or
lateral recess of the sphenoid sinus results in bone remodeling and thinning. Ultimately, a
defect is formed. At this point, the dura herniates through the defect (meningocele). If the
defect is large, brain parenchyma may also herniate through the defect (encephalocele).


Immediate traumatic leaks result from a bony defect or fracture in conjunction with a
dural tear. A possible cause of a delayed traumatic leak is a previously intact dural layer that
has slowly herniated through a bony defect, finally tearing and allowing the cerebrospinal
fluid (CSF) to leak. According to another theory, the tear and bony defect are present from
the time of the original injury, but the leak occurs only after the masking hematoma

Spontaneous CSF rhinorrhea usually manifests in adulthood, coinciding with a

developmental rise in CSF pressure with maturity. The dura of the anterior cranial base is
subject to wide variations in CSF pressure because of several factors, including normal
arterial and respiratory fluctuations. Other stresses include Valsalva-like maneuvers during
nose blowing or straining. This can lead to dural tears in areas of abnormalities of the bony

Increased intracranial pressure is not always present in the case of spontaneous CSF
rhinorrhea. Other proposed mechanisms for nontraumatic CSF leaks include focal atrophy,
rupture of arachnoid projections that accompany the fibers of the olfactory nerve, and
persistence of an embryonic olfactory lumen.

Iatrogenic CSF rhinorrhea results from surgical disruption of the skull base and dura as
previously discussed.


A thorough history is the first step toward accurate diagnosis. The typical history of a
cerebropsinal fluid (CSF) leak is that of clear, watery discharge, usually unilateral. Diagnosis
is made more easily in patients with recent trauma or surgery than in others. Delayed fistulas
are difficult to diagnose and can occur years after the trauma or operation. These cases often
lead to a misdiagnosis of allergic and vasomotor rhinitis. On occasion, the patient has a
history of headache relieved by drainage of CSF. Drainage may be intermittent as the fluid
accumulates in one of the paranasal sinuses and drains externally with changes in head
position (ie, reservoir sign).

A history of headache and visual disturbances suggests increased intracranial pressure.

Sometimes, associated symptoms can assist in localizing the leak. For example, anosmia
(present in 60% of individuals with post-traumatic rhinorrhea), indicates an injury in the
olfactory area and anterior fossa, especially when it is unilateral. Optic nerve deficits suggest
a lesion in the region of tuberculum sellae, sphenoid sinus, or posterior ethmoid cells.
Patients with recurrent meningitis, especially pneumococcal meningitis, should be evaluated
for a defect that exposes the intracranial space to the upper airway, regardless of the presence
or absence of CSF rhinorrhea.

Physical examination

Physical examination should include complete rhinologic (including endoscopic),

otologic, head and neck, and neurologic evaluations. Endoscopy may reveal an encephalocele
or meningocele. Drainage of CSF in some cases may often be elicited on endoscopy by
having the patient perform a Valsalva maneuver or by compressing both jugular veins
(Queckenstedt-Stookey test). However, most of the time physical examination is unrevealing,
especially in patients with intermittent CSF rhinorrhea.

In patients with head trauma, a mixture of blood and CSF may make the diagnosis
difficult. CSF separates from blood when it is placed on filter paper, and it produces a
clinically detectable sign: the ring sign, double-ring sign, or halo sign. However, the presence
of a ring sign is not exclusive to CSF and can lead to false-positive results.[1] In contrast to
unilateral rhinorrhea, bilateral rhinorrhea gives no clue of the laterality of the defect.
However, even in this situation, exceptions can occur. Paradoxical rhinorrhea occurs when
midline structures that act as separating barriers (eg, crista galli, vomer) are dislocated. This
dislocation allows CSF to flow to the opposite side and manifest at the contralateral naris.
The clinical findings most frequently associated with CSF rhinorrhea are meningitis (30%)
and pneumocephalus (30%).


Unless medical or surgical contraindications exist, surgical repair is recommended in all

patients with spontaneous or iatrogenic cerebropsinal fluid (CSF) rhinorrhea in order to
prevent ascending meningitis.

In patients with nonsurgical trauma, waiting a period of 5-7 days to allow conservative
measures (bed rest, stool softeners, and lumbar drainage) to assist with secondary closure of
the traumatic defect is reasonable. However, if CSF rhinorrhea persists beyond this point, or
if a large skull base defect is observed at the time of injury, surgical repair is warranted.

If an iatrogenic leak is detected intraoperatively, it should be repaired at the time of the

original surgery. In most cases of iatrogenic injury presenting in a delayed fashion, surgical
repair is necessary. A lumbar drain placed at the time of repair has not been shown to
decrease recurrence of the CSF leak.

Relevant Anatomy

The most common anatomic sites of spontaneous cerebrospinal fluid (CSF) leaks are the
areas of congenital weakness of the anterior cranial fossa and areas related to the type of
surgery performed. The lateral lamella of the cribriform plate appears to be involved in
approximately 40% of the cases, whereas a defect in the region of the fontal sinus is detected
15% of the time. The sella turcica and sphenoid sinus are involved in 15% of the cases as

Common sites of injury secondary to endoscopic sinus surgery include the lateral lamella
of the cribriform plate and the posterior ethmoid roof near the anterior and medial sphenoid
wall. Rarely, the leak can originate in the middle or posterior cranial fossa and can reach the
nasal cavity by way of the middle ear and eustachian tube. These patients typically present
with aural fullness due to a serous middle ear effusion.

Surgical repair of skull base defects resulting in cerebrospinal fluid (CSF) rhinorrhea is
contraindicated in any patient who is not medically stable to undergo a general anesthetic or
comply with postoperative care.

The management of CSF rhinorrhea depends on the cause, location, and severity of the
leak. When trauma is the cause, the interval between trauma and the onset of the leak is
important. The natural history of CSF rhinorrhea is highly dependant on the underlying

Traumatic leaks stop spontaneously in the majority of cases, thus a conservative approach
is best. The leakage stops within 1 week in 70% of patients, within 3 months in 20-30%, and
within 6 months in most patients. The leak almost never recurs. The opposite is true for
nontraumatic leaks, as only one third stop spontaneously. Intermittent leakage over several
years is characteristic.

Laboratory Studies

Glucose content

A rapid but highly unreliable test is glucose-content determination with the use of glucose
oxidase paper. This method of detecting cerebrospinal fluid (CSF) rhinorrhea is not
recommended as a screening or confirmatory laboratory test to detect the presence of CSF in
the nasal cavity for the following reasons:

Reducing substances present in the lacrimal-gland secretions and nasal mucus may
cause false-positive results.

Glucose, at a concentration of 5 mg/dL, can lead to a positive result with this test.

Active meningitis can lower the glucose level in the CSF and may lead to false-
negative readings.

This test is not specific for the side or site of leak.

Beta-trace protein [2]

Also known as prostaglandin D synthase, this protein is synthesized primarily in arachnoid
cells, oligodendrocytes, and the choroids plexus within the CNS. Beta-trace protein is also
present in the human testes, heart, and serum. It is altered by the presence of renal failure,
multiple sclerosis, cerebral infarction, and certain CNS tumors. This test has been used to
diagnose CSF rhinorrhea in multiple studies, with a sensitivity of 92% and specificity of
100%. This test is not specific for side or site of leak and can be difficult to collect if the leak
is intermittent.


Beta2-transferrin is produced by neuraminidase activity within the central nervous system.

Therefore, beta2-transferrin is located only within the CSF, perilymph, and aqueous humor.

The assay has a high sensitivity and specificity, it is performed rapidly, and it is
noninvasive. A minimum of 0.5 mL of fluid is necessary for electrophoresis, but difficulties
in collection of this fluid have been noted, especially in intermittent, low-volume leaks.

Beta2-transferrin is stable at room temperature for approximately 4 hours; therefore,

immediate refrigeration following collection is recommended. Specimens should not be

This is currently single best laboratory test for identifying the presence of CSF in
sinonasal fluid. It should be kept in mind, however, that this test does not provide information
regarding the site or laterality of the defect. Not all centers are capable of testing fluid for
beta2-transferrin; therefore, sending the laboratory specimen out for processing may delay

Imaging Studies

Computed tomography (CT) scanning [3]

High-resolution CT scanning is the imaging modality of choice for identifying a skull base
defect associated with CSF rhinorrhea. CT scans may demonstrate skull base defects
resulting from accidental or iatrogenic trauma, an underlying anatomic or developmental
abnormality, or an erosive lesion such as a neoplasm.

CT scans should be performed in the axial plane with 1 mm (or less) slice thickness and
reformatted into coronal and sagittal planes. The evaluation of congenital defects or
spontaneous defects may be aided by 3-dimensional reconstruction of the bone to permit in-
depth analysis of the floor of the anterior or middle cranial fossa.

Pneumocephalus on a CT scan may indicate a dural tear. A deviated crista galli is a

radiologic sign in patients presenting with primary CSF rhinorrhea; this finding supports a
congenital bony dehiscence as the etiologic basis for this condition. In some circumstances,
an air-fluid level is present in one or more of the sinuses. This is not diagnostic of CSF and
may be the result of acute or chronic inflammation.

High-resolution CT imaging may reveal defects in the skull base that do not leak or are
not sites of active leaking, making the diagnosis more difficult.

Magnetic resonance imaging (MRI)

MRI typically is not recommended as a first-line imaging modality in the evaluation of

CSF rhinorrhea unless an encephalocele is demonstrated on examination or is suspected.
Unlike CT imaging, MRI does not delineate well bony defects within the anterior or middle
cranial fossa. In addition, MRI is more costly and more time consuming. In many instances,
the injection of a contrast agent may be necessary. Similar to CT imaging, MRI may not be

CT cisternography [4]

CT cisternography improves the diagnostic yield of plain CT by injecting intrathecal

contrast to better localize the site of the CSF leak. As opposed to conventional CT imaging,
only one study is typically necessary. CT cisternography depicts the precise location of CSF
rhinorrhea in most patients with active leaks. Patients with intermittent CSF rhinorrhea may
have false-negative CT cisternograms. Another disadvantage of this technique is that it may
miss cribriform or ethmoid sinus defects.

This is an invasive procedure and is not very frequently used. Despite its low morbidity, it
can be associated with nausea, headaches, and acute organic psychosyndromes.

MR cisternography [5]

Avoidance of intrathecal injection of contrast is a key benefit of MR cisternography. T2-

weighted imaging can be used to detect the presence of CSF in the sinonasal cavity without
the invasiveness of contrast injection. Pulse sequences performed during MRI can be
designed so as to enhance the probability of detecting CSF within the sinonasal cavity. As
with CT cisternography, false-negative studies may result when CSF rhinorrhea is

Nuclear medicine studies

Radioactive isotopes can be introduced into the CSF by means of a lumbar or suboccipital
puncture. Serial scanning or scintiphotography can then be used to determine the distribution
of these agents.

A commonly used adjunct is the placement of nasal pledgets in various high-risk areas.
These pledgets then can be analyzed for the presence of the tracer. Different tracers,
including radioactive iodine-131, radioactive iodinated serum albumin (RISA), ytterbium-
169, diethylenetriamine pentaacetic acid (DTPA), indium-111 DTPA, technetium-99m
human serum albumin, and99m Tc pertechnetate can be used. Despite their relative safety,
studies based on these tracers have several limitations, including the following:

Precise localization of the defect site is difficult

The isotope is absorbed into the circulatory system and can contaminate extracranial

Patient positioning can cause distal pledgets to incorrectly absorb the isotope.

False-positive results are present in as many as 33% patients.

Borderline readings are not reliable. A high reading of radioactivity is necessary to

diagnose a true leak.

For further information, please see Cerebrospinal Fluid Leak Imaging in the Radiology

Diagnostic Procedures

The injection of intrathecal fluorescein has been used to diagnose and localize the site(s)
of cerebrospinal fluid (CSF) rhinorrhea.[6]

The injection of intrathecal fluorescein is commonly used to diagnose and localize the
site(s) of CSF rhinorrhea. However, the US Food and Drug Administration has not approved
the use of fluorescein for this purpose.
A lumbar puncture and/or placement of a subarachnoid lumbar drain is used to facilitate
the injection. After puncture or drain placement, 10 mL of CSF is withdrawn in a sterile
fashion. Precisely 0.1 mL of 10% nonophthalmic fluorescein solution is diluted in the 10 mL
of CSF. The mixture is then reinjected into the subarachnoid space over a period of 10
minutes. The use of this dilution and the slow injection technique help minimize central
potential complications (eg, seizures) that have been previously reported with intrathecal

In most instances, fluorescein is visible with standard xenon light sources used during
endoscopic sinus surgery. However, minute amounts of fluorescein resulting from small bony
defects may be difficulty to detect using a rigid endoscope.

Since the peak absorption of fluorescein occurs at 494 nm, a blue-light filter (440-490 nm
wavelength) can help enhance visualization. This is particularly useful when fluorescein is
filling an encephalocele or in cases of very small leaks that cannot be observed with standard
xenon light sources. See the image below.

After intrathecal fluorescein is administered, an exposed frontal recess encephalocele is seen.

Treatment & Management

Medical Therapy

Conservative management

Conservative treatment has been advocated in cases of immediate-onset cerebrospinal

fluid (CSF) rhinorrhea following accidental trauma, given the high likelihood of spontaneous
resolution of the leak. Conservative management consists of a 7-10 day trial of bed rest with
the head of the bed elevated approximately 15-30. This angle of inclination is sufficient to
reduce the CSF pressure at the basal cisterns. Coughing, sneezing, nose blowing, and heavy
lifting should be avoided as much as possible. Stool softeners should be used to decrease the
strain and increased ICP associated with bowel movements.

A subarachnoid lumbar drain may be placed to drain approximately 5-10 mL of CSF per
hour. Continuous drainage is recommended over intermittent drainage to avoid spikes in CSF
pressure. The utility of a lumbar drain is limited in cases of a large skull base defect or
iatrogenic CSF leaks. The long-term consequences of a persistent defect in the anterior
cranial fossa dissuade many physicians from using this method of treatment.


It is logical to assume that the communication between a sterile environment (intracranial

vault) and a nonsterile environment (sinonasal cavity) will ultimately result in infection of the
sterile compartment. This has led to the use of prophylactic antibiotics in patients with CSF
rhinorrhea. However, no conclusive evidence suggests this practice decreases the risk of
ascending meningitis.

Prior studies assessing the benefits of prophylactic antibiotic use in cases of traumatic CSF
rhinorrhea have yielded mixed results. Two large meta-analyses of patients presenting with
nonsurgical traumatic CSF leaks revealed no difference in the rates of ascending meningitis
in patients treated with prophylactic antibiotics compared with patients treated with
conservative measures alone.
The use of prophylactic antibiotics in patients incurring skull base injuries during
endoscopic sinus surgery has not been studied in a randomized controlled fashion. The
administration of antibiotics in this setting is reasonable because patients undergoing sinus
surgery have underlying inflammatory or infectious pathology. Invasion of the sterile
intracranial compartment with resulting meningitis is a feared complication, which leads to
the commonplace use of antibiotics under these circumstances.


Acetazolamide can be a useful adjunct in the treatment of patients with spontaneous CSF
rhinorrhea associated with elevated intracranial pressure. Acetazolamide is a nonbacteriocidal
sulfonamide that is used primarily as a diuretic, given its ability to inhibit carbonic anhydrase.
It inhibits the reversible conversion of water and CO2 to bicarbonate and hydrogen ions.

The relative deficiency of hydrogen ions within epithelial cells results in decreased Na/K
ATPase activity, which leads to a decreased efflux of water into the CSF. Ultimately, this
reduces the volume of CSF.

A randomized, prospective study by Gosal et al, however, suggested that acetazolamide

may not aid in resolving traumatic CSF rhinorrhea and may instead cause harmful metabolic
and electrolyte disturbances. The study involved 44 patients with head trauma-related CSF
rhinorrhea, 21 of whom received acetazolamide and 23 of whom did not. CSF leaks had a
median duration of 5 days before resolving in the acetazolamide group, compared with 4 days
in the other patients, with the acetazolamide patients demonstrating decreased levels of serum
pH, bicarbonate, and potassium.[7]

The side effects of acetazolamide include weight loss, diarrhea, nausea, metabolic
acidosis, polyuria, and paresthesias, any of which may result in the cessation of therapy.
Metabolic profiles should be monitored on a regular basis to ascertain the effect on serum

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Disorders of Taste and Smell

Introduction and Background


Historically, disorders of taste and smell have been difficult to diagnose and treat, often
because of a lack of knowledge and understanding of these senses and their disease states. An
alteration in taste or smell may be a secondary process in various disease states, or it may be
the primary symptom.

The true prevalence of disorders of taste and smell in the general population is unknown.
The best data available are from a 1994 survey, which revealed that 2.7 million American
adults report an olfactory problem and 1.1 million adults report a gustatory problem.[1] It is
known that individuals tend to underreport olfactory impairment, indicating these values
underestimate the true magnitude of these disorders.

It is also known that chemosensory dysfunction deteriorates with age; given the aging of
the US population, it stands that a significant and increasing number of individuals will
experience age-related sensory loss.[2] A 2002 study showed the prevalence of objective
olfactory impairment in adults older than 53 years is 24.5% and grows more prevalent with
age, to 62.5 % in those aged 80-97 years. Extrapolating from these values, there are currently
14 million older adults with some degree of olfactory impairment. Self-reported impairment
in this study was only 9.5%, which supports the need for more accurate data based on
objective measures.[3]

Fortunately, the National Health and Nutrition Examination Survey (NHANES) adopted
smell and taste testing in January 2013, with plans to release updated data in 2015 regarding
the prevalence and impact of loss of taste and smell across the entire US population.
Loss of smell and/or taste has been linked to inadequate nutritional intake, reduced social
pleasure, and decreased psychological wellbeing. It may even be life threatening, impairing
the detection of smoke in a fire or the ability to identify spoiled food. Because approximately
80% of taste disorders are truly smell disorders, much of this article focuses on the sense of
smell and its dysfunction, with additional discussion of taste and related disorders. See the
image below.

Head anatomy with olfactory nerve.


The disorders of smell are classified as "-osmias" and those of taste as "-geusias."

Anosmia - Inability to detect odors

Hyposmia - Decreased ability to detect odors
Dysosmia - Distorted identification of smell
o Parosmia - Altered perception of smell in the presence of an odor, usually
o Phantosmia Perception of smell without an odor present
o Agnosia - Inability to classify or contrast odors, although able to detect odors
Ageusia - Inability to taste
Hypogeusia - Decreased ability to taste
Dysgeusia Distorted ability to taste

Smell and taste disorders can be total (all odors or tastes), partial (affecting several odors
or tastes), or specific (only one or a select few odors or tastes).
Anatomy and Physiology

Olfactory system

The olfactory neuroepithelium is located at the upper area of each nasal chamber adjacent
to the cribriform plate, superior nasal septum, and superior-lateral nasal wall. It is a
specialized pseudostratified neuroepithelium containing the primary olfactory receptors. In
neonates, this area is a dense neural sheet, but, in children and adults, the respiratory and
olfactory tissues interdigitate. As humans age, the number of olfactory neurons steadily
decreases. In addition to the olfactory neurons, the epithelium is composed of supporting
cells, Bowman glands and ducts unique to the olfactory epithelium, and basal cells that allow
for the regeneration of the epithelium.

The sense of smell is mediated through stimulation of the olfactory receptor cells by
volatile chemicals. To stimulate the olfactory receptors, airborne molecules must pass
through the nasal cavity with relatively turbulent air currents and contact the receptors.
Odorants can also be perceived by entering the nose posteriorly through the nasopharynx to
reach the olfactory receptor via retronasal olfaction. This mechanism is thought to play a key
role in the sensation of flavor during eating and drinking. Odorants diffuse into the mucous
and are transported to the olfactory receptor with the help of odorant-binding proteins.[4]
Important determinants of an odor's stimulating effectiveness include duration, volume, and
velocity of a sniff.

Each olfactory receptor cell is a primary sensory bipolar neuron. The average nasal cavity
contains more than 100 million such neurons. The olfactory neurons are unique because they
are generated throughout life by the underlying basal cells. New receptor cells are generated
approximately every 30-60 days.

Each regenerating receptor cell extends its axon (CN I) into the CNS as a first-order
olfactory neuron and forms synapses with target mitral and tufted cells in the olfactory bulb.

The bipolar olfactory neurons have a short peripheral process and a long central process. The
peripheral process extends to the mucosal surface to end in an olfactory knob, which has
several immobile cilia forming a dense mat at the mucosal surface. The cilia express the
olfactory receptors that interact with odorants. The family of odor receptor proteins are G-
protein coupled receptors (GPCRs) associated with adenylate cyclase. The genes that encode
them were discovered in 1991 by Linda Buck and Richard Axel, culminating in the Nobel
Prize awarded in 2004.

This family encompasses approximately 900 genes, the largest in the genome. It has been
found in mice that each neuron expresses only one gene, so odorants are recognized by the
complex binding pattern they create. This is most likely the case in humans as well.
Interestingly, these genes have been recently discovered to exist in nonolfactory tissues such
as sperm and the gut. The function of these genes outside of their role in olfaction is under

Once an odorant binds to its receptor, a signaling cascade depolarizes the neuron, which
sends the signal along its axon, which then converges together within the bundled axons of
the fila olfactoria deep to the epithelium.

These axons project through the cribriform plate to the ipsilateral olfactory bulb. The
olfactory bulb cells contacted by the olfactory receptor cells include the mitral and tufted
cells, arranged in specialized areas termed glomeruli. The axon terminals of receptorlike
neurons synapse within the same glomeruli, forming an early topographical odorant map.
Therefore, an odor is thought to activate a set of odorant receptors based on its chemical
composition. The corresponding glomeruli of the olfactory bulbs are in turn activated,
creating a unique pattern of excitation in the olfactory bulb for each odorant.

The glomerular cells are the primary output neurons of the olfactory bulb. Axons from
these cells travel to the olfactory cortex, which is divided into 5 parts, including (1) the
anterior olfactory nucleus, connecting the 2 olfactory bulbs through the anterior commissure,
(2) the olfactory tubercle, (3) the pyriform cortex, which is the main olfactory discrimination
region, (4) the cortical nucleus of the amygdala, and (5) the entorhinal area, which projects to
the hippocampus.

The olfactory pathway does not involve a thalamic relay prior to its cortical projections.
Relays from the olfactory tubercle and the pyriform cortex project to other olfactory cortical
regions and to the medial dorsal nucleus of the thalamus and probably involve the conscious
perception of odors.
Conversely, the cortical nucleus of the amygdala and the entorhinal area are limbic system
components and may be involved in the affective, or hedonic, components of odors. Regional
cerebral blood flow (measured with positron emission tomography) is significantly increased
in the amygdala with introduction of a highly aversive odorant, and it is associated with
subjective ratings of perceived aversiveness.

The vomeronasal organ (VNO), or Jacobson organ, is a bilateral membranous structure

located within pits of the anterior nasal septum, deep to the nasal respiratory mucosa and next
to the septal perichondria. Its opening in the nasal vestibule is visible in 91-97% of adult
humans, and it is 2 cm from the nostril at the junction of the septal cartilage with the bony
septum. Unlike lower animals, axons projecting from the VNO have not been found in
postnatal humans.

The VNO is believed by some to detect external chemical signals termed pheromones or
vomeropherins through neuroendocrine-type cells found within the organ. These signals are
not detected as perceptible smells by the olfactory system and may mediate human
autonomic, psychologic, and endocrine responses.

Free trigeminal nerve endings, which are stimulated by aversive or pungent stimuli (eg,
ammonia), exist in the nasal mucosa. These are processed via separate pathways from those
in the olfactory system, described above.

Gustatory system

Taste perception is mediated by individual taste buds, with 50-100 tightly packed cells in
each bud. Taste buds are modified epithelial cells, not direct neurons as in olfactory function.
Taste bud cells are classified into types I-IV and include taste receptor, supporting and basal
progenitor cells.[5] These cells have a life span of approximately 10 days and arise
continuously from the underlying basal cell layer in a process of constant turnover, similar to
olfactory receptor cells. Any bud may contain receptors necessary to identify each different

Afferent nerve branches making synaptic contact with receptor cells penetrate the base of
the taste bud. Taste buds occupy papillae, which are projections embedded in the tongue
epithelium. A single nerve fiber innervates multiple taste papillae, and the nerve contact
exerts trophic influences on the epithelium.

The specificity of the gustatory receptor cells is determined by the epithelium in which it
resides, not by the particular nerve innervating the bud. A single fiber in the chorda tympani
may respond to multiple types of tastes, some tastes more than others. This ability of single
nerve fibers to respond to multiple types of stimuli is referred to as broad tuning, and it is
shared by the olfactory system.

Lingual papillae have the following 4 forms, each occupying different areas of the tongue:

Fungiform papillae are located in the anterior two thirds of the tongue. People have an
average of 33 fungiform papillae with approximately 114 buds per papilla.
Innervation is through cranial nerve (CN) VII via the chorda tympani.
Circumvallate papillae are located in the posterior two thirds of the tongue, consisting
of 8-12 papillae, approximately 250 buds each, for an average of 3000 total buds.
Cranial nerve IX innervates these, along with the entire posterior one third of the
Foliate papillae reside in folds and clefts at the lateral borders of the tongue, with
approximately 1280 buds. Cranial nerve IX innervates these buds.
Filiform papillae have no taste buds.

Other locations of taste buds include the following:

Soft palate - Innervated by CN VII via the greater superficial petrosal nerve
Epiglottis and larynx - Supplied by the superior laryngeal branch of CN X
Pharynx - Supplied by branches from CN IX and CN X

Free trigeminal nerve endings exist on the tongue; these detect strong, often displeasing or
irritating sensations in the oral cavity.

Five different taste qualitiessalty, sweet, sour, bitter, and umami (monosodium
glutamate/5' nucleotide)have been identified. In addition, there is evidence that another
taste perception exists, the ability to sense lipid content. Similar to odorant transmission, most
tastes are mediated by various GPCRs. Sweet, umami, and bitter are detected by members of
2 GPCR families, taste 1 receptor family (TAS1R) and taste 2 receptor family (TAS2R).
Lipid content is mediated by a free fatty acid receptor. In contrast, sour and salty are mainly
mediated by ion channels.[6]

Ongoing research has identified odor and taste receptors in surprising places, including
skeletal muscle, brain, respiratory tract, and GI tract. Evidence shows taste receptors present
from the stomach to the colon function in nutrient sensing.[7] The exact role of these receptors
in regions other than the nose and mouth needs to be further elucidated. Doing so offers
promise in terms of our understanding of human physiology and targets for novel therapeutic

Etiology of Smell and Taste Disorders

Olfactory dysfunction

Disturbances in olfaction can result from pathologic processes at any level along the
olfactory pathway. They can be classified in a way analogous to otologic dysfunction, as
conductive or sensorineural defects. In conductive (ie, transport) defects, transmission of an
odorant stimulus to the olfactory neuroepithelium is disrupted. Sensorineural defects involve
the more central neural structures. Overall, the most common causes of primary olfactory
deficits are aging, nasal and/or sinus disease, prior viral upper respiratory tract infections
(URTIs), and head trauma.[8]

Conductive defects

Inflammatory processes cause a large portion of olfactory defects. These may include
rhinitis of various types, including allergic, acute, or toxic (eg, cocaine use). Chronic
rhinosinusitis causes progressive mucosal disease and often leads to decreased olfactory
function despite aggressive allergic, medical, and surgical intervention.

Masses may block the nasal cavity, preventing the flow of odorants to the olfactory
epithelium. These include nasal polyps (most common), inverting papilloma, or any nasal

Developmental abnormalities (eg, encephaloceles, dermoid cysts) also may cause

Patients with laryngectomies or tracheotomies experience hyposmia because of a reduced
or absent nasal airflow. Children with tracheotomies who are cannulated very young and for a
long period may have a continued problem with olfaction even after decannulation because of
a lack of early stimulation of the olfactory system.

Central/sensorineural defects

Infectious and inflammatory processes contribute to central defects in olfaction and in

transmission. These include viral infections (which may damage the neuroepithelium),
sarcoidosis (affecting neural structures), Wegener granulomatosis, and multiple sclerosis.
Once thought to be mostly a conductive defect through mucosal edema and polyp formation,
chronic rhinosinusitis also appears to disrupt the neuroepithelium with irreversible loss of
olfactory receptors through up-regulated apoptosis.

Head trauma, brain surgery, or subarachnoid hemorrhage may stretch, damage, or transect
the delicate fila olfactoria or damage brain parenchyma and result in anosmia.[9]

Sense of smell decreases with age, and it has been shown that the number of fibers in the
olfactory bulb decreases throughout one's lifetime. In one study the average loss in human
mitral cells was 520 cells per year with a reduction in bulb volume of 0.19 mm 3.[10] These
olfactory bulb losses may be secondary to sensory cell loss in the olfactory mucosa and/or
general decline in the regenerative process from stem cells in the subventricular zone.

Congenital syndromes may be associated with neural losses. Kallmann syndrome is one
type of congenital smell loss and is due to failed olfactory structure ontogenesis and
hypogonadotropic hypogonadism. One study found the vomeronasal organ to be absent in
patients with Kallmann syndrome.

Endocrine disturbances (eg, hypothyroidism, hypoadrenalism, diabetes mellitus) may

affect olfactory function.

Toxicity of systemic or inhaled drugs (eg, aminoglycosides, formaldehyde) can contribute

to olfactory dysfunction. Many other medications and compounds may alter smell sensitivity,
including alcohol, nicotine, organic solvents, and direct application of zinc salts.[11]
Over-the-counter zinc nasal sprays have been implicated in the cause of smell loss. On
June 16, 2009, the US Food and Drug Administration (FDA) issued a public health advisory
and notified consumers and healthcare providers to discontinue use of intranasal zinc
products. The intranasal zinc products (Zicam Nasal Gel/Nasal Swab products by Matrixx
Initiatives) are herbal cold remedies that claim to reduce the duration and severity of cold
symptoms and are sold without a prescription. The FDA received more than 130 reports of
anosmia (inability to detect odors) associated with intranasal zinc. Many of the reports
described the loss of smell with the first dose.[12]

Smoking has not been shown conclusively to reduce olfactory function, although some
studies have shown a correlation with reduced sense of smell and smoking. That
withstanding, research has identified squamous metaplasia and change in the morphology of
the olfactory receptor neurons and a higher level of apoptosis of these neurons in smokers
compared with controls. In addition, there is evidence that the volume of the olfactory bulb is
reduced in smokers.[13]

Various neuropsychiatric disorders (eg depression, schizophrenia, seasonal affective

disorder) have been linked to hyposmia. It has been shown that patients with acute major
depressive disorder have reduced olfactory sensitivity and reduced olfactory bulb volumes.[14]
Schizophrenia patients have also been shown to have decreased olfactory bulb volume and
impaired odor detection abilities compared with controls.[15] The neurologic explanation for
these findings is under active investigation and may lead to new therapies or early detection
screening tools.

Degenerative processes of the central nervous system (eg, Parkinson disease, Alzheimer
disease) and other neurologic diseases (Huntington disease, multiple sclerosis, motor neuron
disease) have been associated with hyposmia. Alzheimer and Parkinson patients show
changes in detection, discrimination, and identification of odors compared with age-matched
controls. The severity of dysfunction is correlated to disease progression. In most cases,
olfactory loss is present years before motor or cognitive symptoms. However, this is usually a
gradual loss and often goes unnoticed or unreported by patients.

The assessment of olfactory function should become a more standard aspect of patient
evaluation. There are numerous functional and structural approaches available to assess the
olfactory system, including psychosocial and electrophysiological testing, as well as imaging
studies. Objective measures of olfactory function may serve as an early marker for these
diseases or as a prognostic indicator. An understanding of the mechanism of the decrease in
smell could help to further elucidate the pathophysiology of these disorders or uncover new
treatments.[16, 17]

Gustatory dysfunction

Much of what is perceived as a taste defect is truly a primary defect in olfaction resulting
in an alteration of flavor. The components that comprise the sensation of flavor include the
food's smell, taste, texture, and temperature. Each of these sensory modalities is stimulated
independently to produce a distinct flavor when food enters the mouth.

Taste may be enhanced by tongue movements, which increase the distribution of the
substance over a greater number of taste buds. Adaptation in taste perception exerts a greater
influence than in other sensory modalities.

Other than smell dysfunction, the most frequent causes of taste dysfunction are prior
URTI, head injury, and idiopathic causes, but many other causes can be responsible.

Lesions at any site from the mucosa, taste buds, unmyelinated nerves, or cranial nerves to
the brain stem may impair gustation.

Oral cavity and mucosal disorders including oral infections, inflammation, and radiation-
induced mucositis can impair taste sensation. The site of injury with radiotherapy is probably
the microvilli of the taste buds, not the taste buds themselves, since taste buds are thought to
be radioresistant.

Poor oral hygiene is a leading cause of hypogeusia and cacogeusia. Viral, bacterial,
fungal, and parasitic infections may lead to taste disturbances because of secondary taste bud

Normal aging produces taste loss due to changes in taste cell membranes involving altered
function of ion channels and receptors rather than taste bud loss.[2, 18]
Malignancies of the head and neck, as well as of other sites, are associated with decreased
appetite and inability to appreciate flavors.

Use of dentures or other palatal prostheses may impair sour and bitter perception, and
tongue brushing has been shown to decrease taste acuity.

Surgical manipulation may alter taste permanently or temporarily. Resection of the tongue
and/or portions of the oral cavity, most commonly for reasons of malignancy, decreases the
number of taste buds. Radiation and chemotherapy damage taste receptors and decrease
salivary flow, altering taste perception. In otologic surgery, stretching or transection of the
chorda tympani nerve may result in temporary dysgeusia. Bilateral injury still may not result
in permanent taste dysfunction, because of the alternate innervation through the otic ganglion
to the geniculate ganglion via the greater superficial petrosal nerve.

Gastric bypass surgery can also have adverse olfactory and gustatory effects. In a study by
Graham et al of 103 patients who underwent Roux-en-Y gastric bypass, sensory changes in
taste and smell were reported by 73% and 42% of these individuals, respectively.[19]

Nutritional deficiencies are involved in taste aberrations. Decreased zinc, copper, and
nickel levels can correlate with taste alterations. Nutritional deficiencies may be caused by
anorexia, malabsorption, and/or increased urinary losses.

Endocrine disorders also are involved in taste and olfactory disorders. Diabetes mellitus,
hypogonadism, Sjogrens and pseudohypoparathyroidism may decrease taste sensation, while
hypothyroidism and adrenal cortical insufficiency may increase taste sensitivity. Hormonal
fluctuations in menstruation and pregnancy also influence taste.

AIDS patients often complain of alterations in taste, and detection thresholds of glutamic
acid and hydrochloride are higher in patients suffering from AIDS.[20]

Heredity is involved in some aspects of gustation. The ability to taste phenylthiourea

(bitter) and other compounds with an N-C= group is an autosomal dominant trait. Studies
have shown that phenylthiourea tasters detect saccharin, potassium chloride (KCl), and
caffeine as more bitter. Type I familial dysautonomia (ie, Riley-Day syndrome) causes severe
hypogeusia or ageusia because of the absence of taste bud development.
Direct nerve or CNS damage, as in multiple sclerosis, facial paralysis, and thalamic or
uncal lesions, can decrease taste perception.

Many other diseases can affect gustation (eg, lichen planus, aglycogeusia, Sjgren
syndrome, renal failure with uremia and dialysis, erythema multiforme, geographic tongue,

Diagnosis of Smell and Taste Disorders

The first step in diagnosing any deficit of taste and smell is obtaining a thorough history
and physical examination. Give attention to any antecedent URI, nasal or sinus pathology,
history of trauma, other medical problems, and medications taken.

Order sinus CT scans if the history and examination are not consistent with a common
pattern (eg gradually progressing olfactory loss in a 38-year-old male). Generally, olfactory
loss in the absence of CNS symptoms or an abnormal neurologic examination is highly
unlikely to be associated with an intracranial mass such as a meningioma. However, an MRI
of the brain is often recommended when the history is not straightforward or a secondary
neurologic symptom or sign is obtained (eg, 50-year-old woman with a taste phantom that
does not resolve after 6 months). Although a standard laboratory panel is not recommended,
tests to evaluate for allergy, diabetes mellitus, thyroid functions, renal and liver function,
endocrine function, and nutritional deficiencies may be obtained based on history and the
physical examination. Olfactory epithelium biopsy is used primarily as a research technique.

Clinical measurement of olfaction

Quantitative measurement of smell and taste dysfunctions is most important when

chemosensory dysfunction is the primary symptom. The major goal of sensory testing is to
assess the degree of chemosensory dysfunction.

Clinical testing can be time consuming and difficult to perform precisely, but some
commercially available tests attempt to simplify and standardize these efforts.
Tests of olfactory function that evaluate threshold of odor detection and odor
identification have been developed that can provide a reliable measure of olfactory ability.
These tests include butanol threshold test, the University of Pennsylvania Smell Identification
Test (UPSIT) (Sensonics, Inc., and the Sniffin' Sticks test (Burghart
Messtechnik GmbH Another test, the olfactory-evoked response, has
been used in research centers along with odor identification tests to evaluate aberrant
olfaction with relation to neurologic disease.

Butanol threshold test

The butanol threshold test involves a forced-choice test using an aqueous concentration of
butyl alcohol in one sniff bottle and water in the other. The patient is asked to identify the
bottle containing the odorant, with each nostril tested separately.

After each incorrect response, the concentration of butanol is increased by a factor of 3

until the patient either achieves 5 correct responses or fails to correctly identify the bottle
with 4% butanol.

The detection threshold is recorded as the concentration at which the patient correctly
identifies the butanol on 5 consecutive trials. The scoring relates the patient's threshold to a
normal subject population

University of Pennsylvania Smell Identification Test

The UPSIT involves 40 microencapsulated odors in a scratch-and-sniff format, with 4

response alternatives accompanying each odor. The patient takes the test alone, with
instructions to guess if not able to identify the item.

Anosmic patients tend to score at or near chance (10/40 correct). The scores are compared
against sex- and age-related norms, and the results are analyzed. This test has excellent test-
retest reliability.

A chart is available relating scores to varying patient populations, including patients with
multiple sclerosis, with Korsakoff syndrome, and those feigning anosmia. Those in the latter
group tend to score much lower on the test than expected by chance.
Cross-Cultural Smell Identification Test

A variant of the UPSIT, which can be given in 5 minutes, was proposed for a quick
measure of olfactory function. The 12-item Cross-Cultural Smell Identification Test (CC-
SIT) was developed using input on the familiarity of odors in several countries, including
China, Colombia, France, Germany, Italy, Japan, Russia, and Sweden.

The odorants chosen include banana, chocolate, cinnamon, gasoline, lemon, onion, paint
thinner, pineapple, rose, soap, smoke, and turpentine. Representatives from each country
identified these odorants most consistently.

This test is an excellent alternative for measuring olfactory function in the clinical setting,
especially when time is limited, since it is rapid and reliable.

The disadvantage of this test is that its brevity limits its sensitivity in detecting subtle
changes in olfactory function.

Sniffin' Sticks

These use a series of reusable penlike odor-dispensing devices and tests odor the threshold
through a single staircase method, odor discrimination with forced choice among 3 of 16
different common odorants, and odor identification with multiple forced choice from 4 verbal
items. A composite score is calculated from a composite of all 3 scores to provide an overall
evaluation of olfactory function.

Olfactory-evoked response (usually reserved for research studies)

To standardize the patient reaction to eye movements, electroencephalogram (EEG)

electrodes and an electrooculogram measure olfactory-evoked potentials. A visual tracking
task is performed to ensure constant alertness to the task, and headphones playing white noise
are worn to mask auditory clues.

Either carbon dioxide (no odor but a trigeminal stimulant) or hydrogen sulfide is delivered
via an olfactometer to the nose in a constantly flowing air stream. N1 is the first negative
peak measured, and P2 is the second positive trough. Latencies are measured to these 2
In patients with neurologic disease, the UPSIT revealed abnormality more frequently than
olfactory-evoked responses.

For clinical olfactory function testing, the authors' experience is that the self-administered
UPSIT test allows for practical use during a busy clinical practice. However, in the absence
of the olfactory tests described above, a simple screening test using a common alcohol pad
can be used. The envelope is opened at one end and presented to the patient. With the
patient's eyes closed, the pad is then positioned at the level of the umbilicus and slowly
brought closer to the nose. The patient is instructed to notify the tester when the alcohol is
again detected. The distance of the pad from the nose correlates with the patient's olfactory
ability, with a distance of less than 20 cm indicating hyposmia.

Clinical measurement of taste

Evaluation of taste disorders is not as well developed as that of olfaction. It involves

measurement of detection or recognition thresholds. No comparable approach to odor
identification tests is available because only 5 basic taste sensations exist and only 4 of these
(sweet, salty, bitter, and sour) are tested.

Salivary adaptation and size of the tongue area stimulated influence the threshold
assessment. Thus, these tests are extremely variable. Changes in threshold detection do not
necessarily indicate correlation to changes in suprathreshold taste intensity. Testing of the
taste thresholds alone does not provide a full picture of the level of gustatory function or
dysfunction. For example, a patient after radiation therapy may recover recognition
thresholds for the 4 taste qualities, but the magnitude of the perceived tastes still may be quite

Threshold detection

Taste Strips (Burghart, Messtechnik, Germany) are strips of paper that can be purchased
and are already impregnated with 4 taste qualities: sweet, sour, salty, and bitter, each of these
containing 4 different concentrations resulting in 16 strips in total. Specifically, these are
sweet (0.4, 0.2, 0.1, 0.05 g/mL sucrose), sour (0.3, 0.165, 0.09, 0.05 g/mL citric acid), salty
(0.25, 0.1, 0.04, 0.016 g/mL sodium chloride), and bitter (0.006, 0.0024, 0.0009, 0.0004 g/mL
quinine hydrochloride). Normative values for these strips are available.
Magnitude matching

Suprathreshold testing involves assessment of the patient's perceptions of taste intensities

at levels above threshold. One method of measuring this quality is with a psychophysical
procedure known as magnitude matching.

Other tests of suprathreshold tastes have involved assigning numbers to their sensations,
but no direct comparison across individuals can be made. Specific numbers, such as 10 or
100, do not have any intrinsic psychologic value.

Conversely, magnitude matching makes use of one sensory modality that is presumed to
be normal (in this case, hearing) in comparison to a deficiency in another sensory modality
(taste) by using the following procedure:

Several concentrations of sodium chloride, sucrose, citric acid, and quinine hydrochloric
acid, along with several loudness levels of a 1000-Hz tone, are provided for the magnitude
matching task. The patient sips each solution and expectorates, and the tones are presented
via headphones. The patient provides estimates of perceived magnitude for each stimulus.
The results are scaled in relation to loudness functions to reveal abnormalities of taste as
depressed psychophysical functions. In other words, patients with hypogeusia associate
stronger taste concentrations with weaker tones than normal patients. The major limitations
of this testing modality are its dependence on normal hearing and its complicated design,
which takes a significant amount of time to administer and analyze.

Spatial test

Taste function in the various areas of the tongue and oral cavity can be measured using a
spatial test. Because the gustatory system is multiply innervated, damage to one of the 3
major nerves (ie, chorda tympani, glossopharyngeal, greater superficial petrosal) or their
ganglia may cause a disturbance of taste that can be evaluated only by testing the anatomic
areas supplied by those nerves.

To test these areas, 4 standardized sizes of filter paper are soaked with strong concentrations
of the 4 basic tastes. The papers are randomly placed on the 4 quadrants of the tongue and on
both sides of the soft palate. Patients then identify the quality of the taste and rate its intensity
using the same scale as in whole mouth assessment.
Treatment of Olfactory and Gustatory Dysfunction

Treatment of olfactory dysfunction

Any treatment of olfactory disorders must first treat the specific causative abnormality if it
has been identified from diagnostic tests, history, and physical examination.

Local nasal and/or sinus conditions should be optimally managed with saline lavage,
decongestants, antihistamines, antibiotics, and/or nasal and systemic steroids, if applicable.
Polyps and sinus disease that are resistant to medical management should be surgically
addressed to remove the conductive defect. Care must be exercised during surgery to avoid
damage to the olfactory regions.

Aggressive treatment of these disorders, if present, provides a good chance of

improvement. In general, conductive olfactory losses are the most amenable to treatment.

A few of the sensorineural olfactory defects also have specific treatments, but these are
fewer and have less chance of success. Generally, viral processes that damage the olfactory
neuroepithelium, sarcoidosis, and multiple sclerosis do not have specific remedies; however,
steroids may be administered in an attempt to limit the inflammation.

Endocrine disturbances may be addressed by administration of the deficient hormone, as

with hypothyroidism. Control of diabetes mellitus may slow neural degeneration of the
olfactory system. However, in a study of 12 males with Kallmann syndrome, Gong and Gao
stated that, while the condition can be effectively treated with the administration of human
chorionic gonadotropin (hCG), human menopausal gonadotropin (hMG), and testosterone
undecanoate, there is currently no effective therapy for the olfactory dysfunction occurring in
this disease.[21]

Idiopathic cases of olfactory loss are not amenable to specific treatment, although some
unproven remedies have been attempted. The best known of these is zinc sulfate. It has not
been proven beneficial and is generally regarded as ineffective.

Other unproven remedies include pharmacologic doses of vitamins, topical steroids, and
tricyclic antidepressants (for their effect on CSF catecholamines).
A viral URTI can cause extensive scarring and replacement of the olfactory
neuroepithelium with respiratory epithelium, but studies suggest that stem cells remain,
allowing for potential regeneration of the olfactory epithelium. Recovery of smell in these
cases can take weeks to months and, in some instances, may never occur. It is now known
that olfactory training is safe and effective therapy for postinfectious olfactory loss. This
method involves the patient choosing 4 known odors and intentionally sniffing these same 4
odors twice daily. A recent randomized, controlled study showed improved olfactory function
after 18 weeks, particularly in patients who started olfactory training within the first 12
months after onset.[22] Eliminating toxins (eg, cigarette smoke, airborne pollutants) may help.

Overall, the patient with olfactory disorders needs reassurance that these generally are not
life-threatening problems and that many other individuals experience them. In some patients,
psychiatric evaluation and treatment may be warranted. Most importantly, the physician is
responsible for warning the patient with olfactory disorders of the hazards associated with the
inability to smell odors such as smoke, natural gas leaks, and spoiled food. Smoke detectors,
as well as natural gas and propane gas detectors, are commercially available to help eliminate
such risks.

Treatment of gustatory dysfunction

As with olfactory problems, direct initial treatment of gustatory dysfunction toward the
causative abnormality, if possible. Address any nasal pathology causing decreased olfaction
and thus affecting flavor perception.

Treat mucosal disorders (eg, infections, inflammations). Treat oral candidiasis and other
local factors, and replete any vitamin deficiency that may cause glossitis.

Aid patients in eliminating local irritants (eg, mouthwashes, ill-fitting dentures). In

mucositis or dry mouth as a result of radiation therapy, artificial saliva or salivary stimulants
and local anti-inflammatory medications may improve some taste dysfunction.

Correcting endocrine disorders with the appropriate hormone replacement may improve
the taste disorder. Consider eliminating a medication suspected of causing dysgeusia unless
the medication is crucial in treating another medical problem and cannot be substituted.
In the case of familial dysautonomia, in which patients have a complete lack of lingual
taste buds, subcutaneous administration of methacholine has been reported to normalize
previously elevated taste thresholds for all taste qualities. The cholinergic mechanism is
probably related to taste transduction via free nerve endings because these patients have no
taste receptors.

Some gustatory deficits are untreatable (eg, some cases of nerve or CNS damage, end-
stage diabetic neuropathy, multiple sclerosis).

Advise patients that chewing food well increases the release of the tastant and increases
saliva production to further distribute the chemicals. Switching foods during the meal
decreases the phenomenon of adaptation and can improve detection of the tastes.

Finally, for patients who are anosmic or hyposmic (including many elderly people),
simulated odors are available to use while cooking to augment the sensation of flavor. A
drawback of these simulated odors is that, to normosmic people, the smell is quite pungent.
Thus, these odors cannot be used in mixed groups of anosmic and normosmic individuals.


Smell and taste disorders traditionally have been overlooked in most aspects of medical
practice because these specialized senses often are not considered critical to life. However,
they affect everyday enjoyment of food, and they impair detection of the potentially
dangerous smells of smoke or spoiled food.

Anxiety and depression, as well as anorexia and nutritional deficiencies, may result from
taste and smell disorders. Many causes of smell and taste disorders exist, and the modalities
of treatment begin with treating the specific deficit, if possible.

Unfortunately, much about the diagnosis and treatment of taste and smell dysfunction
remains to be discovered. Most "taste" defects are truly alterations in perception of flavor due
to smell defects, and they should be treated accordingly.

Some standardized tests, such as the butanol threshold, odor identification, Sniffin' Sticks,
UPSIT, and olfactory-evoked potentials, can help diagnose and measure olfactory
Reassurance is one of the most important aspects of treatment in these disorders because
cures are often difficult to obtain and spontaneous resolution may take weeks, months, or


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Epistaxis, or bleeding from the nose, is a common complaint. It is rarely life threatening
but may cause significant concern, especially among parents of small children.[1] Most
nosebleeds are benign, self-limiting, and spontaneous, but some can be recurrent. Many
uncommon causes are also noted.

Epistaxis can be divided into 2 categories, anterior bleeds and posterior bleeds, on the
basis of the site where the bleeding originates (see the image below).

Posterior epistaxis from the left sphenopalatine artery.

The true prevalence of epistaxis is not known, because most episodes are self-limited and
thus are not reported. When medical attention is needed, it is usually because of either the
recurrent or severe nature of the problem. Treatment depends on the clinical picture, the
experience of the treating physician, and the availability of ancillary services.[2, 3, 4, 5]

Also see Anterior Epistaxis Nasal Pack, Posterior Epistaxis Nasal Pack, and Surgery for
Pediatric Epistaxis.


The nose has a rich vascular supply, with substantial contributions from the internal
carotid artery (ICA) and the external carotid artery (ECA).

The ECA system supplies blood to the nose via the facial and internal maxillary arteries.
The superior labial artery is one of the terminal branches of the facial artery. This artery
subsequently contributes to the blood supply of the anterior nasal floor and anterior septum
through a septal branch.

The internal maxillary artery enters the pterygomaxillary fossa and divides into 6
branches: posterior superior alveolar, descending palatine, infraorbital, sphenopalatine,
pterygoid canal, and pharyngeal.

The descending palatine artery descends through the greater palatine canal and supplies
the lateral nasal wall. It then returns to the nose via a branch in the incisive foramen to
provide blood to the anterior septum. The sphenopalatine artery enters the nose near the
posterior attachment of the middle turbinate to supply the lateral nasal wall. It also gives off a
branch to provide blood supply to the septum.

The ICA contributes to nasal vascularity through the ophthalmic artery. This artery enters
the bony orbit via the superior orbital fissure and divides into several branches. The posterior
ethmoid artery exits the orbit through the posterior ethmoid foramen, located 2-9 mm anterior
to the optic canal. The larger anterior ethmoid artery leaves the orbit through the anterior
ethmoid foramen.

The anterior and posterior ethmoid arteries cross the ethmoid roof to enter the anterior
cranial fossa and then descend into the nasal cavity through the cribriform plate. Here, they
divide into lateral and septal branches to supply the lateral nasal wall and the septum.
The Kiesselbach plexus, or Littles area, is an anastomotic network of vessels located on
the anterior cartilaginous septum. It receives blood supply from both the ICA and the ECA.[6]
Many of the arteries supplying the septum have anastomotic connections at this site.


Bleeding typically occurs when the mucosa is eroded and vessels become exposed and
subsequently break. More than 90% of bleeds occur anteriorly and arise from Littles area,
where the Kiesselbach plexus forms on the septum.[7, 8]
The Kiesselbach plexus is where
vessels from both the ICA (anterior and posterior ethmoid arteries) and the ECA
(sphenopalatine and branches of the internal maxillary arteries) converge. These capillary or
venous bleeds provide a constant ooze, rather than the profuse pumping of blood observed
from an arterial origin. Anterior bleeding may also originate anterior to the inferior turbinate.

Posterior bleeds arise further back in the nasal cavity, are usually more profuse, and are
often of arterial origin (eg, from branches of the sphenopalatine artery in the posterior nasal
cavity or nasopharynx). A posterior source presents a greater risk of airway compromise,
aspiration of blood, and greater difficulty controlling bleeding.


Causes of epistaxis can be divided into local causes (eg, trauma, mucosal irritation, septal
abnormality, inflammatory diseases, tumors), systemic causes (eg, blood dyscrasias,
arteriosclerosis, hereditary hemorrhagic telangiectasia), and idiopathic causes. Local trauma
is the most common cause, followed by facial trauma, foreign bodies, nasal or sinus
infections, and prolonged inhalation of dry air. Children usually present with epistaxis due to
local irritation or recent upper respiratory infection (URI).

In a retrospective cohort study of 2405 patients with epistaxis (3666 total episodes),
Purkey et al used multivariate analysis to identify a series of risk factors for nosebleeds. The
likelihood of epistaxis was found to increase in patients with allergic rhinitis, chronic
sinusitis, hypertension, hematologic malignancy, coagulopathy, or, as mentioned, hereditary
hemorrhagic telangiectasia. The investigators also found increased nosebleeds in association
with older age and colder weather.[9]

Self-induced trauma from repeated nasal picking can cause anterior septal mucosal
ulceration and bleeding. This scenario is frequently observed in young children. Nasal foreign
bodies that cause local trauma (eg, nasogastric and nasotracheal tubes) can be responsible for
rare cases of epistaxis.

Acute facial and nasal trauma commonly leads to epistaxis. If the bleeding is from minor
mucosal laceration, it is usually limited. However, extensive facial trauma can result in severe
bleeding requiring nasal packing. In these patients, delayed epistaxis may signal the presence
of a traumatic aneurysm.

Patients undergoing nasal surgery should be warned of the potential for epistaxis. As with
nasal trauma, bleeding can range from minor (due to mucosal laceration) to severe (due to
transection of a major vessel).

Dry weather

Low humidity may lead to mucosal irritation. Epistaxis is more prevalent in dry climates
and during cold weather due to the dehumidification of the nasal mucosa by home heating


Topical nasal drugs such as antihistamines and corticosteroids may cause mucosal
irritation. Especially when applied directly to the nasal septum instead of the lateral walls,
they may cause mild epistaxis. Medications such as nonsteroidal anti-inflammatory drugs
(NSAIDs) are also frequently involved.

Septal abnormality

Septal deviations (deviated nasal septum) and spurs may disrupt the normal nasal airflow,
leading to dryness and epistaxis. The bleeding sites are usually located anterior to the spurs in
most patients. The edges of septal perforations frequently harbor crusting and are common
sources of epistaxis.


Bacterial, viral, and allergic rhinosinusitis causes mucosal inflammation and may lead to
epistaxis. Bleeding in these cases is usually minor and frequently manifests as blood-streaked
nasal discharge.
Granulomatosis diseases such as sarcoidosis, Wegener granulomatosis, tuberculosis,
syphilis, and rhinoscleroma often lead to crusting and friable mucosa and may be a cause of
recurrent epistaxis.

Young infants with gastroesophageal reflux into the nose may have epistaxis secondary to


Benign and malignant tumors can manifest as epistaxis. Affected patients may also present
with signs and symptoms of nasal obstruction and rhinosinusitis, often unilateral. Intranasal
rhabdomyosarcoma, although rare, often begins in the nasal, orbital, or sinus area in children.
Juvenile nasal angiofibroma in adolescent males may cause severe nasal bleeding as the
initial symptom.

Blood dyscrasias

Congenital coagulopathies should be suspected in individuals with a positive family

history, easy bruising, or prolonged bleeding from minor trauma or surgery. Examples of
congenital bleeding disorders include hemophilia and von Willebrand disease.[6]

Acquired coagulopathies can be primary (due to the diseases) or secondary (due to their
treatments). Among the more common acquired coagulopathies are thrombocytopenia and
liver disease with its consequential reduction in coagulation factors. Even in the absence of
liver disease, alcoholism has also been associated with coagulopathy and epistaxis. Oral
anticoagulants predispose to epistaxis.

Vascular abnormalities

Arteriosclerotic vascular disease is considered a reason for the higher prevalence of

epistaxis in elderly individuals. Hereditary hemorrhagic telangiectasia (HHT; also known as
Osler-Weber-Rendu syndrome) is an autosomal dominant disease associated with recurrent
bleeding from vascular anomalies. The condition can affect vessels ranging from capillaries
to arteries, leading to the formation of telangiectasias and arteriovenous malformations.
Pathologic examination of these lesions reveals a lack of elastic or muscular tissue in the
vessel wall. As a result, bleeding can occur easily from minor trauma and tends not to stop
Various organ systems such as the respiratory, gastrointestinal, and genitourinary systems
may be involved. The epistaxis in these individuals is variable in severity but is almost
universally recurrent.

Other vascular abnormalities that predispose to epistaxis include vascular neoplasms,

aneurysms, and endometriosis.


Children with migraine headaches have a higher incidence of recurrent epistaxis than
children without the disease.[10] The Kiesselbach plexus, which is part of the
trigeminovascular system, has been implicated in the pathogenesis of migraine.[11]


The relationship between hypertension and epistaxis is often misunderstood. Patients with
epistaxis commonly present with an elevated blood pressure. Epistaxis is more common in
hypertensive patients, perhaps owing to vascular fragility from long-standing disease.

Hypertension, however, is rarely a direct cause of epistaxis. More commonly, epistaxis

and the associated anxiety cause an acute elevation of blood pressure. Therapy, therefore,
should be focused on controlling hemorrhage and reducing anxiety as primary means of
blood pressure reduction.

A study by Sarhan and Algamal, which included 40 patients with epistaxis and 40
controls, reported that the number of attacks of epistaxis was higher in patients with a history
of hypertension, but the investigators were unable to determine whether a definite link existed
between nosebleeds and high blood pressure. They did find, however, that control of epistaxis
was more difficult in hypertensive patients; patients whose systolic blood pressure was higher
at presentation tended to need management with packing, balloon devices, or cauterization.[12]

Excessive coughing causing nasal venous hypertension may be observed in pertussis or

cystic fibrosis.

Idiopathic causes

The cause of epistaxis is not always readily identifiable. Approximately 10% of patients
with epistaxis have no identifiable causes even after a thorough evaluation.[13]

The frequency of epistaxis is difficult to determine because most episodes resolve with
self-treatment and, therefore, are not reported.[14] However, when multiple sources are
reviewed, the lifelong incidence of epistaxis in the general population is about 60%, with
fewer than 10% seeking medical attention.[6, 15, 14]

The age distribution is bimodal, with peaks in young children (2-10 y) and older
individuals (50-80 y). Epistaxis is unusual in infants in the absence of a coagulopathy or nasal
pathology (eg, choanal atresia, neoplasm). Local trauma (eg, nose picking) does not occur
until later in the toddler years. Older children and adolescents also have a less frequent
incidence. Consider cocaine abuse in adolescent patients. Prevalence of epistaxis tends to be
higher in males (58%) than in females (42%).


For most of the general population, epistaxis is merely a nuisance. However, the problem
can occasionally be life-threatening, especially in elderly patients and in those patients with
underlying medical problems. Fortunately, mortality is rare and is usually due to
complications from hypovolemia, with severe hemorrhage or underlying disease states.

Overall, the prognosis is good but variable; with proper treatment, it is excellent. When
adequate supportive care is provided and underlying medical problems are controlled, most
patients are unlikely to experience any rebleeding. Others may have minor recurrences that
resolve spontaneously or with minimal self-treatment. A small percentage of patients may
require repacking or more aggressive treatments.

Patients with epistaxis that occurs from dry membranes or minor trauma do well, with no
long-term effects. Patients with HHT tend to have multiple recurrences regardless of the
treatment modality. Patients with bleeding from a hematologic problem or cancer have a
variable prognosis. Patients who have undergone nasal packing are subject to increased
morbidity. Posterior packing can potentially cause airway compromise and respiratory
depression. Packing in any location may lead to infection.

Patient Education

For patient education resources, see the Breaks, Fractures, and Dislocations Center, as
well as Broken Nose.
The following precautions should be imparted to the patient:

Use nasal saline spray.

Avoid hard nose blowing or sneezing.

Sneeze with the mouth open.

Do not use nasal digital manipulation.

Avoid hot and spicy foods.

Avoid taking hot showers.

Avoid aspirin and other NSAIDs.

The following simple instructions for self-treatment for minor epistaxis should be provided:

Apply firm digital pressure for 5-10 minutes.

Use an ice pack.

Practice deep, relaxed breathing.

Use a topical vasoconstrictor.


Controlling significant bleeding or hemodynamic instability should always take

precedence over obtaining a lengthy history. Ask specific questions about the severity,
frequency, duration, and laterality of the nosebleed. Determine whether the bleed occurs after
exercise or during sleep or is associated with a migraine. Determine whether hematemesis or
melena has occurred because posterior bleeding in particular may present in this fashion.

Inquire about precipitating and aggravating factors and methods used to stop the bleeding.
Most nosebleeds are reported as spontaneous events and are frequently related to nose
picking or other trauma; therefore, investigate the various possibilities.

Foreign bodies inserted in the nose may also present with epistaxis, but bleeding may be
less and accompanied by foul or purulent discharge if the object has been retained for some
time. A unilateral nasal discharge suggests the presence of a foreign body.
Children easily can insert small batteries from electronic devices (eg, calculators, watches,
handheld video games) into their nostrils. Not only can local irritation and bleeding result, but
these can leak and cause a chemical alkali burn that may result in local tissue necrosis. Severe
complications (eg, nasal stenosis) can result from batteries. Removal is a priority; removing
the batteries within 4 hours of insertion is best.

In addition to obtaining a head and neck history with an emphasis on nasal symptoms,
elicit a general medical history concerning relevant medical conditions, current medications,
and smoking and drinking habits.

Inquire about previous epistaxis, hypertension, hepatic or other systemic disease, easy
bruising, or prolonged bleeding after minor surgical procedures. A history of frequent
recurrent nosebleeds, easy bruising, or other bleeding episodes should make the clinician
suspicious of a systemic cause and prompt a hematologic workup. Obtain any family history
of bleeding disorders or leukemia.

Children with severe epistaxis are more likely to have required nasal cauterization, an
underlying coagulopathy, a positive family history of bleeding, and anemia. Although
unusual, children with bleeding disorders (eg, von Willebrand disease) can occasionally have
normal coagulation profiles. More than 1 sample may be required to notice the abnormality
due to biologic variability throughout the day.

Use of medicationsespecially aspirin, NSAIDs, warfarin, heparin, ticlopidine, and

dipyridamoleshould be documented, as these not only predispose to epistaxis but make
treatment more difficult. Particularly in children, include investigation of suspicion of
accidental ingestion (eg, accidental ingestion of rat poison in toddlers).

Physical Examination

Before evaluating a patient with epistaxis, have sufficient illumination, adequate suction,
all the necessary topical medications, and cauterization and packing materials ready. Remove
all packings, even though bleeding may not be active. The importance of obtaining adequate
anesthesia and vasoconstriction if time permits cannot be overemphasized. A comfortable
patient tends to be more cooperative, allowing for better examination and more effective
Perform a thorough and methodical examination of the nasal cavity. Blowing the nose
decreases the effects of local fibrinolysis and removes clots, permitting a better examination.
Application of a vasoconstrictor (eg, 0.05% oxymetazoline) before the examination may
reduce hemorrhage and help to pinpoint the precise bleeding site. A topical anesthetic (eg,
4% aqueous lidocaine) reduces pain associated with the examination and nasal packing. Clots
are then suctioned out to permit a thorough examination.

Gently insert a nasal speculum (see the image below) and spread the naris vertically.
Begin the examination with inspection, looking specifically for any obvious bleeding site on
the septum that may be amenable to direct pressure or cautery. This permits visualization of
most anterior bleeding sources. Anterior bleeds from the nasal septum are most common
type, and the site can frequently be identified if bleeding is active.

Nasal speculum.

If an anterior source cannot be visualized, if the hemorrhage is from both nares, or if

constant dripping of blood is seen in the posterior pharynx, the bleeding may be from a
posterior site. After placement of an anterior pack, and, if bleeding is noted in the pharynx
with the anterior pack in place, strongly consider a posterior bleed.

Massive epistaxis may be confused with hemoptysis or hematemesis. Blood dripping from
the posterior nasopharynx confirms a nasal source. Approximately 90% of nosebleeds can be
visualized in the anterior portion of the nasal cavity.
Fiberoptic endoscopy may be performed with a flexible or (preferably) rigid endoscope to
inspect the entire nasal cavity, including the nasopharynx. The rigid endoscope is preferred
because of its superior optics and its ability to allow endoscopic suction and cauterization.

Examine the skin for evidence of bruises or petechiae that may indicate an underlying
hematologic abnormality.

Assess vital signs. Although high blood pressure rarely, if ever, causes epistaxis on its
own, it may impede clotting. Check blood pressure, and complete a workup if high blood
pressure is present. Persistent tachycardia must be recognized as an early indicator of
significant blood loss requiring intravenous (IV) fluid replacement and, potentially,


Complications of epistaxis may include the following:


Septal hematoma/perforation

External nasal deformity

Mucosal pressure necrosis

Vasovagal episode

Balloon migration


Diagnostic Considerations

Recurrent epistaxis in children could be caused by a foreign body, especially if the

nosebleeds are accompanied by symptoms of unilateral nasal congestion and purulent
rhinorrhea. Delayed epistaxis in a trauma patient may signal the presence of a traumatic

Other conditions to be considered include the following:

Chemical irritants
Hepatic failure



Heparin toxicity

Ticlopidine toxicity

Dipyridamole toxicity



Differential Diagnoses

Allergic Rhinitis


Cocaine Toxicity

Coumarin Plant Poisoning

Disseminated Intravascular Coagulation in Emergency Medicine

Emergent Treatment of Endometriosis

Nasal Foreign Bodies

Nonsteroidal Anti-inflammatory Agent Toxicity

Pediatric Osler-Weber-Rendu Syndrome

Rodenticide Toxicity

Salicylate Toxicity

Sinusitis Imaging

Type A Hemophilia

Type B Hemophilia
von Willebrand Disease

Warfarin and Superwarfarin Toxicity

Approach Considerations

For the most part, laboratory studies are not needed or helpful for first-time nosebleeds or
infrequent recurrences with a good history of nose picking or trauma to the nose. However,
they are recommended if major bleeding is present or if a coagulopathy is suspected.

Laboratory Tests

Laboratory tests to evaluate the patients condition and underlying medical problems may
be ordered depending on the clinical picture at the time of presentation. If the bleeding is
minor and not recurrent, then a laboratory evaluation may not be needed.

If a history of persistent heavy bleeding is present, obtain a hematocrit count and type and
cross-match. If a history of recurrent epistaxis, a platelet disorder, or neoplasia is present,
obtain a complete blood count (CBC) with differential. The bleeding time is an excellent
screening test if suspicion of a bleeding disorder is present. Obtain the international
normalized ratio (INR)/prothrombin time (PT) if the patient is taking warfarin or if liver
disease is suspected. Obtain the activated partial thromboplastin time (aPTT) as necessary.

Other Studies

Direct visualization with a good directed light source, a nasal speculum, and nasal suction
should be sufficient in most patients. However, computed tomography (CT) scanning,
magnetic resonance imaging (MRI) or both may be indicated to evaluate the surgical
anatomy and to determine the presence and extent of rhinosinusitis, foreign bodies, and
neoplasms. Nasopharyngoscopy may also be performed if a tumor is the suspected cause of
bleeding. Sinus films are rarely indicated for a nosebleed. Angiography is rarely indicated.

Treatment & Management

Approach Considerations
When medical attention is needed for epistaxis, it is usually because of the problem is
either recurrent or severe. Treatment depends on the clinical picture, the experience of the
treating physician, and the availability of ancillary services.

In most patients with epistaxis, the bleeding responds to cauterization, nasal packing, or
both. For those who have recurrent or severe bleeding for which medical therapy has failed,
various surgical options are available. After surgery or embolization, patients should be
closely observed for any complications or signs of rebleeding.

Medical approaches to the treatment of epistaxis may include the following:

Adequate pain control in patients with nasal packing, especially in those with
posterior packing (However, the need of adequate pain control has to be balanced
with the concern over hypoventilation in the patient with posterior pack.)

Oral and topical antibiotics to prevent rhinosinusitis and possibly toxic shock

Avoidance of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs)

Medications to control underlying medical problems (eg, hypertension, vitamin K

deficiency) in consultation with other specialists

Also see Anterior Epistaxis Nasal Pack, Posterior Epistaxis Nasal Pack, and Surgery for
Pediatric Epistaxis.

Manual Hemostasis

Initial treatment begins with direct pressure. The nostrils are squeezed together for 5-30
minutes straight, without frequent peeking to see if the bleeding is controlled. Usually, 5-10
minutes is sufficient.

Patients should keep their heads elevated but not hyperextended because hyperextension
may cause bleeding into the pharynx and possible aspiration. This maneuver works more than
90% of the time.

If direct pressure is not sufficient, gauze moistened with epinephrine at a ratio of 1:10,000
or phenylephrine (Neo-Synephrine) may be placed in the affected nostril to help vasoconstrict
and achieve hemostasis.
Humidification and Moisturization

If bleeding is caused by excessive dryness in the home (eg, from radiator heating), patients
may benefit from humidifying the air with a cool mist vaporizer in the bedroom or, as a
simpler alternative, placing a metal basin of water on top of a radiator to humidify the
ambient air.

Nasal saline sprays are useful. Oxymetazoline may also be used, with fewer cardiac
adverse effects. To minimize the risk of rhinitis medicamentosa and tachyphylaxis, these
agents should be used for no more than 3-5 days at a time.

The physician may consider local application of bacitracin or petrolatum ointment directly
to the Kiesselbach area with a cotton applicator to prevent further drying (studies recommend
2 wk).


Bleeding from the Kiesselbach plexus (Littles area) is frequently treated with silver
nitrate cauterization.[13] Manage the vessels leading to the site before managing the actual
bleeding site. Avoid random and aggressive cauterization and cautery on opposing surfaces
of the septum.

Electrocauterization with an insulated suction cautery unit can also be used. This method
is usually reserved for more severe bleeding and for bleeding in more posteriorly located
sites, and it often requires local anesthesia. The effectiveness of both cauterization methods
can be enhanced by using rigid endoscopy, especially in the case of more posteriorly located
bleeding sites (see the image below).[16]
Resolved posterior epistaxis after endoscopic cauterization of the left sphenopalatine artery.

After the bleeding has been controlled, instruct the patient to use nasal saline spray and
antibiotic ointment and to avoid strenuous activities for 7-10 days. NSAIDs are to be avoided
if at all possible. Digital manipulation of the nose is to be avoided. A topical vasoconstrictor
may be used if minor bleeding recurs with the dislodging of the eschar.

Nasal Packing

Nasal packing can be used to treat epistaxis that is not responsive to cauterization. Two
types of packing, anterior and posterior, can be placed. In both cases, adequate anesthesia and
vasoconstriction are necessary.

A study by Kundi and Raza suggested that in patients with epistaxis, removal of nasal
packs after 12 hours leads to a lower incidence of headache and excessive lacrimation than
does removal of packs after 24 hours, with no significant difference in bleeding recurrence.
The study involved 60 patients with epistaxis, evenly divided between the 12-hour and 24-
hour groups.[17]


For anterior packing, various packing materials are available. Petroleum jelly gauze (0.5 in
72 in) filled with an antibiotic ointment is traditionally used (see the image below). Layer it
tightly and far enough posteriorly to provide adequate pressure. Blind packing with loose
gauze is to be avoided.

Vaseline gauze packing.

Merocel sponges can be placed relatively easily and quickly but may not provide adequate
pressure (see the image below). They should be coated with an antibiotic ointment and can be
hydrated with a topical vasoconstrictor.

Expandable (Merocel) packing (dry).

All packings should be removed in 3-4 days. Absorbable materials (eg, Gelfoam, Surgicel,
Avitene) may be used in patients with coagulopathy to prevent trauma upon packing removal.
Administer prophylactic antibiotics to all patients with packing, and instruct them to avoid
physical strain for 1 week.
Also see Anterior Epistaxis Nasal Pack.


Epistaxis that cannot be controlled by anterior packing can be managed with posterior
packing. Classically, rolled gauzes are used, but medium tonsil sponges can be substituted.

Recently, inflatable balloon devices (eg, 12 or 14 French Foley catheters) or specially

designed catheters manufactured by companies such as Storz and Xomed (eg, Storz Epistaxis
Catheter, Xomed Treace Nasal Post Pac) have become popular because they are easier to
place. Avoiding overinflation of the balloon is important because it can cause pain and
displacement of the soft palate inferiorly, interfering with swallowing.

A 2010 study by Garcia Callejo et al determined that gauze packing, despite being slower
and more uncomfortable, has a higher success rate, produces fewer local injuries, and costs
less than inflatable balloon packing.[18]

Regardless of the type of posterior pack used, an anterior pack should also be placed.
Admit all patients with posterior packing to the intensive care unit (ICU) for close monitoring
of oxygenation, fluid status, and pain control. An antibiotic should also be given to prevent
rhinosinusitis and possible toxic shock syndrome.

Also see Posterior Epistaxis Nasal Pack.

Management of packing failure

Packing failure can be caused by inadequate placement resulting either from lack of
patient cooperation (especially in the pediatric age group) or from anatomic factors (eg,
deviated septum). In cases of packing failure, a careful endoscopic examination with the
patient under general anesthesia may be considered. Bleeding sites can be cauterized under
endoscopic guidance, a deviated septum can be straightened, spurs can be removed, and
meticulous packing can be placed.[19]

If these steps fail to control the bleeding, arterial ligation (see below) may be performed at
the same time.

Arterial Ligation
The choice of the specific vessel or vessels to be ligated depends on the location of the
epistaxis. In general, the closer the ligation is to the bleeding site, the more effective the
procedure tends to be.

External carotid artery

Ligation of the external carotid artery (ECA) can be performed with the patient under
local or general anesthesia. A horizontal skin incision is made between the hyoid bone and
the superior border of the thyroid cartilage. Subplatysmal skin flaps are then raised, and the
sternocleidomastoid muscle is retracted posteriorly.

Next, the carotid sheath is opened and its contents exposed. The ECA is identified by
following the internal carotid artery (ICA) for a few centimeters and dissecting the ECA
beyond its first few branches. After the ECA has been positively identified, it is usually
ligated just distal to the superior thyroid artery. Continued bleeding after ligation may be
from anastomoses with the opposite carotid system or the ipsilateral ICA.

Internal maxillary artery

Internal maxillary artery ligation has a higher success rate than ECA ligation because of
the more distal site of intervention. Traditionally, the internal maxillary artery is accessed
transantrally via a Caldwell-Luc approach. With the help of an operating microscope, the
posterior sinus wall is removed in a piecemeal fashion, and the posterior periosteum is
carefully opened. The internal maxillary artery and 3 of its terminal branches (ie,
sphenopalatine, descending palatine, pharyngeal) are elevated with nerve hooks, then clipped.
The posterior sinus wall is then packed with Gelfoam, and the gingivobuccal incision is

More recently, transoral and transnasal endoscopic approaches have been described. The
transoral approach is useful in patients with midface trauma, hypoplastic antra, or maxillary

In the transoral approach, the buccinator space is first entered through a gingivobuccal
incision. The buccal fat pad is removed, and the attachment of the temporalis to the coronoid
process is identified. This process facilitates the identification of the internal maxillary artery.
The vessel is then doubly clipped and divided. This procedure has a higher failure rate than
the transantral approach because the site of ligation is more proximal.

The transnasal endoscopic method requires skills with endoscopic instruments. A large
middle meatal antrostomy is made to expose the posterior sinus wall. The middle turbinate
can be partially resected to ensure adequate exposure. The remaining steps are similar to
those of the traditional transantral approach.

Endoscopic technique can also be used to ligate the sphenopalatine artery at its exit from
the sphenopalatine foramen.[20, 21]
An incision is made just posterior to the posterior
attachment of the middle turbinate. The mucosal flap is then carefully elevated to reveal the
sphenopalatine artery, which is then clipped and ligated.

Ethmoid artery

If bleeding occurs high in the nasal vault, consider ligation of the anterior ethmoid artery,
the posterior ethmoid artery, or both. These arteries are approached through an external
ethmoidectomy incision.

The anterior ethmoid artery is usually found approximately 22 mm (range, 16-29 mm)
from the anterior lacrimal crest. If clipping the artery does not stop the bleeding, then the
posterior ethmoid artery may be ligated. This artery is found approximately 12 mm posterior
to its anterior counterpart. It should be clipped, not cauterized, because it is only 4-7 mm
anterior to the optic nerve.


Bleeding from the ECA system may be controlled with embolization, either as a primary
modality in poor surgical candidates or as a second-line treatment in those for whom surgery
has failed. Patients considered candidates for embolization should be transferred to hospitals
with interventional radiology capability.[19]

Preembolization angiography is performed to check for the presence of any unsafe

communications between the ICA and ECA systems. Selective embolization of the internal
maxillary artery[22] and sometimes the facial artery may be performed. Postprocedure
angiography can be used to evaluate the degree of occlusion. The most common reason for
failure is continued bleeding from the ethmoid arteries.
Palliative Therapy for Hereditary Hemorrhagic Telangiectasia

Management of hereditary hemorrhagic telangiectasia (HHT) is palliative because the

underlying defect is not curable. Options include coagulation with potassium-titanyl-
phosphate (KTP) or neodymium:yttrium-aluminum-garnet (Nd:YAG) lasers,
septodermoplasty, embolization, and estrogen therapy.[23]

Complications of Treatment

Potential treatment complications include the following :

Cauterization - Synechia, septal perforation

Anterior packing - Synechia, rhinosinusitis, toxic shock syndrome, eustachian tube

dysfunction, scarring of the nasal ala and columella

Posterior packing - Synechia, rhinosinusitis, toxic shock syndrome, eustachian tube

dysfunction, dysphagia, scarring of nasal ala and columella, hypoventilation, sudden

Transantral internal maxillary artery ligation - Anesthetic risks, rhinosinusitis,

oroantral fistula, infraorbital numbness, dental injury

Transoral internal maxillary artery ligation - Anesthetic risks, cheek numbness,

trismus, tongue paresthesia

Anterior or posterior ethmoid artery ligation - Anesthetic risks, rhinosinusitis, lacrimal

duct injury, telecanthus, blindness

Embolization - Facial pain, trismus, facial paralysis, skin necrosis, blindness, stroke,
groin hematoma

Dietary Measures

Few dietary measures are indicated. Patients should avoid hot and spicy foods and drink
plenty of fluids.

Activity Restriction
Patients should avoid strenuous activities, hot showers, and digital trauma. They should
use nasal saline spray liberally and should employ digital pressure and ice packs as needed
for minor recurrences.

Prevention of Epistaxis

To the extent possible, patients should avoid the following:

Strenuous activities - Protection from direct trauma from some sports activities is
afforded by the use of helmets or face pieces.

Hot and dry environments The effects of such environments can be mitigated by
using humidifiers, better thermostatic control, saline spray, and antibiotic ointment on
the Kiesselbach area.

Hot and spicy foods

Digital trauma In children, nose picking is difficult to deter and should probably be
considered inevitable. Keeping the childs nails well trimmed may be helpful.

Nose blowing and excessive sneezing - Instruct patients to sneeze gently with the
mouth open.

Inappropriate or careless use of drugs - Consider drug education relating to use or

accidental ingestion of aspirin, warfarin (eg, rat poison in toddlers), or drug abuse in


A hematologist may have to be consulted. Consultation with an interventional radiologist

may also be appropriate.

Long-Term Monitoring

Use supportive measures to prevent recurrence (eg, nasal saline spray, Bactroban nasal
ointment). Arrange for follow-up care to remove packing in 3-4 days.


Medication Summary
Most patients with epistaxis who seek medical attention are likely to be treated with
cauterization, anterior packing, or both. Those with severe or recalcitrant bleeding may need
posterior packing, arterial ligation, or embolization. Pharmacotherapy plays only a supportive
role in treating the patient with epistaxis.

Topical vasoconstrictors

Class Summary

Topical vasoconstrictors act on alpha-adrenergic receptors in the nasal mucosa, causing

vessels to constrict.

Oxymetazoline 0.05% (Afrin)

Oxymetazoline is applied directly to mucous membranes, where it stimulates alpha-

adrenergic receptors and causes vasoconstriction. Decongestion occurs without drastic
changes in blood pressure, vascular redistribution, or cardiac stimulation.

Oxymetazoline can be used in combination with lidocaine 4% to provide effective nasal

anesthesia and vasoconstriction.


Class Summary

When anesthetics are used concomitantly with vasoconstrictors, their anesthetic effect is
prolonged and the pain threshold increased.

Lidocaine 4% (Xylocaine)

Lidocaine decreases permeability to sodium ions in neuronal membranes. This results in

the inhibition of depolarization, blocking the transmission of nerve impulses. Lidocaine can
be used in combination with oxymetazoline 0.05% to provide effective nasal anesthesia and

Antibiotic ointments

Class Summary

Antibiotic ointments help prevent local infection and provide local moisturization.
Mupirocin ointment 2% (Bactroban nasal)

Mupirocin ointment inhibits bacterial growth by inhibiting RNA and protein synthesis. It is a
compounded medication.

Cauterizing agents

Class Summary

Cauterizing agents coagulate cellular proteins, which can in turn reduce bleeding.

Silver nitrate

Silver nitrate coagulates cellular protein and removes granulation tissue. It also has
antibacterial effects.


1. Moreau S, De Rugy MG, Babin E, Courtheoux P, Valdazo A. Supraselective

embolization in intractable epistaxis: review of 45 cases. Laryngoscope. 1998 Jun.
108(6):887-8. [Medline].

2. Abelson TI. Epistaxis. Schaefer SD. Rhinology and Sinus Disease 1st ed. New York:
Mosby; 1998. 43-50.

3. Douglas R, Wormald PJ. Update on epistaxis. Curr Opin Otolaryngol Head Neck
Surg. 2007 Jun. 15(3):180-3. [Medline].

4. Emanuel JM. Epistaxis. Cummings CW. Otolaryngology-Head and Neck Surgery. 3rd
ed. St. Louis: Mosby; 1998. 852-865.
5. Pope LE, Hobbs CG. Epistaxis: an update on current management. Postgrad Med J.
2005 May. 81(955):309-14. [Medline]. [Full Text].

6. Cummings CW. Epistaxis. Cummings. Otolaryngology: Head and Neck Surgery. 4th
ed. Philadelphia, Pa: Elsevier, Mosby; 2005. Chap 40.

7. Padgham N. Epistaxis: anatomical and clinical correlates. J Laryngol Otol. 1990 Apr.
104(4):308-11. [Medline].

8. Guarisco JL, Graham HD 3rd. Epistaxis in children: causes, diagnosis, and treatment.
Ear Nose Throat J. 1989 Jul. 68(7):522, 528-30, 532 passim. [Medline].

9. Purkey MR, Seeskin Z, Chandra R. Seasonal variation and predictors of epistaxis.

Laryngoscope. 2014 Mar 15. [Medline].

10. Jarjour IT, Jarjour LK. Migraine and recurrent epistaxis in children. Pediatr Neurol.
2005 Aug. 33(2):94-7. [Medline].

11. Knight YE, Goadsby PJ. The periaqueductal grey matter modulates trigeminovascular
input: a role in migraine?. Neuroscience. 2001. 106(4):793-800. [Medline].

12. Sarhan NA, Algamal AM. Relationship between epistaxis and hypertension: a cause
and effect or coincidence?. J Saudi Heart Assoc. 2015 Apr. 27 (2):79-84. [Medline].

13. Qureishi A, Burton MJ. Interventions for recurrent idiopathic epistaxis (nosebleeds) in
children. Cochrane Database Syst Rev. 2012 Sep 12. 9:CD004461. [Medline].

14. Gifford TO, Orlandi RR. Epistaxis. Otolaryngol Clin North Am. 2008 Jun. 41(3):525-
36, viii. [Medline].

15. Schlosser RJ. Clinical practice. Epistaxis. N Engl J Med. 2009 Feb 19. 360(8):784-9.

16. Durr DG. Endoscopic electrosurgical management of posterior epistaxis: shifting

paradigm. J Otolaryngol. 2004 Aug. 33(4):211-6. [Medline].

17. Kundi NA, Raza M. Duration of nasal packs in the management of epistaxis. J Coll
Physicians Surg Pak. 2015 Mar. 25 (3):202-5. [Medline].
18. Garca Callejo FJ, Muoz Fernndez N, Achiques Martnez MT, Fras Moya-Angeler
S, Montoro Elena MJ, Algarra JM. [Nasal packing in posterior epistaxis. Comparison
of two methods]. Acta Otorrinolaringol Esp. 2010 May-Jun. 61(3):196-201.

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States: A Study of the Nationwide Inpatient Sample 2003-2010. J Vasc Interv Radiol.
2013 May 3. [Medline].

20. Abdelkader M, Leong SC, White PS. Endoscopic control of the sphenopalatine artery
for epistaxis: long-term results. J Laryngol Otol. 2007 Aug. 121(8):759-62.

21. Wormald PJ, Wee DT, van Hasselt CA. Endoscopic ligation of the sphenopalatine
artery for refractory posterior epistaxis. Am J Rhinol. 2000;Jul-Aug. 14(4):261-264.

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1995 Dec. 113(6):674-8. [Medline].

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haemorrhagic telangiectasia with intranasal bevacizumab. Br J Haematol. 2013 May
14. [Medline].

Functional Endoscopic Sinus Surgery


Introduction to Functional Endoscopic Sinus Surgery

Rhinology and sinus surgery have undergone a tremendous expansion since the discourses
of Messerklinger and Wigand in the late 1970s.[1, 2, 3]
Imaging advances, increased
understanding of the anatomy and the pathophysiology of chronic sinusitis, and image-guided
surgery have allowed surgeons to perform more complex procedures with increased safety.

Outstanding short- and long-term results have been reported in the literature. Senior et al
reported that symptoms improved in 66 of 72 (91.6%) patients following endoscopic sinus
surgery, with a mean follow-up time of 7.8 years.[4] In addition, endoscopic sinus surgery
significantly influences quality of life; Damm et al reported an improvement in quality of life
for 85% of their patient population, with a mean follow-up time of 31.7 months.[5]

Although functional endoscopic sinus surgery is the primary approach used today for the
surgical treatment of chronic sinusitis, the time-honored external approaches still play a role.
Therefore, familiarity with endoscopic and external approaches, in conjunction with a precise
understanding of the anatomy, ensures optimal patient care and outcome.

A recently developed alternative to functional endoscopic sinus surgery is balloon

sinuplasty. This technique uses balloon catheters to dilate the maxillary, frontal, and sphenoid
natural ostia without bone or soft-tissue removal. Reports show persistent patient symptom
improvement and sinus ostia patency. Further study and long-term outcomes with this
technology will determine its role in endoscopic sinus surgery.[6]

Indications for Endoscopic Sinus Surgery

Endoscopic sinus surgery is most commonly performed for inflammatory and infectious
sinus disease. The most common indications for endoscopic sinus surgery are as follows:

Chronic sinusitis refractory to medical treatment

Recurrent sinusitis

Nasal polyposis

Antrochoanal polyps

Sinus mucoceles

Excision of selected tumors

Cerebrospinal fluid (CSF) leak closure

Orbital decompression (eg, Graves ophthalmopathy)

Optic nerve decompression

Dacryocystorhinostomy (DCR)

Choanal atresia repair

Foreign body removal

Epistaxis control

Typically, endoscopic sinus surgery is reserved for patients with documented

rhinosinusitis, based on a thorough history and a complete physical examination, including
CT scans if appropriate, and in whom appropriate medical treatment has failed.

Medical therapy alone may be inadequate for treatment of nasal polyposis. Aukema et al
found that although 12 weeks of treatment with fluticasone propionate nasal drops reduced
the need for sinus surgery in patients with nasal polyposis and chronic rhinosinusitis, 14 of 27
patients still required surgery.[7] Similarly, antrochoanal polyps require surgical removal.

Nasal masses

Increasingly, selected nasal masses and tumors are being removed endoscopically.
Endoscopic removal of inverted papilloma is controversial. Endoscopic surgery can be
performed for limited lesions in which definitive control and margins can be obtained
endoscopically; this circumstance can be predicted preoperatively via nasal endoscopy and

More extensive lesions should be approached externally; either a lateral rhinotomy method
or a midfacial degloving method can be used for en bloc tumor removal. Further research
with long-term monitoring in this area will better delineate the optimal treatment for these

Cerebrospinal fluid leaks

CSF leaks associated with CSF rhinorrhea can be managed endoscopically. Success rates
of 80% have been reported in the literature with primary endoscopic attempts; success rates
increase to 90% if revision endoscopic closures are included.

With endoscopic repair of CSF leaks, the more extensive neurosurgical external
approaches via craniotomy can be avoided. In certain clinical settings, endonasal
encephaloceles are repaired via endoscopic approaches.

Ophthalmic procedures
Endoscopic approaches may also be applied for ophthalmic procedures, including orbital
decompression, endoscopic DCR, and optic nerve decompression for traumatic indirect optic
neuropathy. Traditionally, these procedures were performed through external approaches, but
as clinical experience in nasal endoscopic techniques has increased, they are now performed
endoscopically. Only surgeons with extensive training in, and expertise with, endoscopic
techniques should perform these procedures.

Contraindications to Endoscopic Sinus Surgery

Certain sinus conditions may not respond completely to endoscopic treatment; these
include intraorbital complications of acute sinusitis, such as orbital abscess or frontal
osteomyelitis with Potts puffy tumor. An open approach, with or without additional
endoscopic assistance, may be preferable in these instances. A careful review of preoperative
CT or magnetic resonance imaging (MRI) scans helps guide the surgeon.

After 2 failures to endoscopically manage CSF leaks associated with CSF rhinorrhea,
patients should be referred to a neurosurgeon for closure using a neurosurgical approach.
Likewise, after failure to endoscopically manage frontal sinus disease, open approaches
should be considered.

Clinical Evaluation

The cornerstone of accurate diagnosis and treatment of chronic sinusitis is a thorough

history and a complete physical examination, including nasal endoscopy. Surgery should not
be considered unless the evaluation clearly identifies chronic sinusitis as the cause of the
patient's constellation of symptoms.

The history should elucidate the frequency of infections, the type and the duration of
symptoms, and the response to medical therapy. Patients with chronic or recurrent symptoms
typically report the following symptoms:

Nasal congestion

Purulent drainage

Postnasal drip

Facial pressure and headache

Hyposmia or anosmia

Nasal obstruction

However, other conditions can mimic chronic sinusitis, causing 1 or more of the above
symptoms. Therefore, ruling out other etiologies for the patient's symptoms is imperative. For
example, patients with allergic rhinitis may have similar problems, such as sneezing, watery
eyes, itchy eyes, nasal congestion, and postnasal drip. If the patient's only problem is allergic
rhinitis, then endoscopic sinus surgery is not the solution, and proper medical treatment
should be prescribed.

A physical examination is an excellent adjunct to patient history in diagnosing or

excluding chronic sinusitis. A complete head and neck examination, along with anterior
rhinoscopy, should be performed. If further nasal examination is required, a full nasal
endoscopy should be carried out. The patient should be assessed for the following conditions:

Septal deviation

Turbinate hypertrophy

Nasal polyps

Nasal airway problems, including dynamic internal or external valve collapse

Ostiomeatal complex, if visible

Adenoidal hypertrophy

Rigid nasal endoscopy with mild septal deviation is depicted in the videos below. Rigid
nasal endoscopy performed in the clinic. A mild left septal deviation is seen anteriorly. The
left middle turbinate and middle meatus are normal. Video courtesy of Vijay R
Ramakrishnan, MD.

Rigid nasal endoscopy. The right side contains normal turbinates and middle meatus with
a small amount of mucus in the inferior meatus. The endoscopy concludes with visualization
of the soft palate, nasopharynx, and Eustachian tube orifices. Video courtesy of Vijay R
Ramakrishnan, MD.
Percussion of the sinuses to elicit tenderness may provide additional information;
however, this is an imperfect technique in terms of sensitivity and specificity.

Patients with suspicious findings on history and physical examination should undergo
computed tomography (CT) scanning. In patients with normal findings on paranasal sinus CT
scans and no change in symptoms after undergoing medical treatment, a diagnosis of chronic
sinusitis is suspect at best. These patients should not be offered functional endoscopic sinus
surgery as a treatment for their symptoms.

Relevant Anatomy

Intimate knowledge and understanding of the anatomy of the lateral nasal wall and the
sinuses (see the image below), in conjunction with a careful preoperative review of CT scans,
are paramount in the safe and complete performance of endoscopic sinus surgery. The
following description of endonasal anatomy is roughly based on the order of dissection
during nasal endoscopy and surgery.

Lateral nasal wall anatomy and paranasal sinus ostia.

Nasal septum and inferior turbinate

Immediately upon entering the nasal cavity, the first structures encountered are the nasal
septum and the inferior turbinate. The nasal septum consists of the quadrangular cartilage
anteriorly, extending to the perpendicular plate of the ethmoid bone posterosuperiorly and the
vomer posteroinferiorly.

Recognizing deflections of the nasal septum preoperatively is important because they may
significantly contribute to nasal obstruction and limit endoscopic visualization during
surgery. As appropriate, patients with septum deflections may be counseled regarding the
need for septoplasty in conjunction with functional endoscopic sinus surgery.

The inferior turbinate extends along the inferior lateral nasal wall posteriorly toward the
nasopharynx. In patients with a significant allergic component to their problems, the inferior
turbinates may be edematous. These patients may benefit from a turbinate reduction at the
same time as the endoscopic sinus surgery. The inferior meatus, where the nasolacrimal duct
opens, is located approximately 1 cm beyond the most anterior edge of the inferior turbinate.

Middle turbinate

As the endoscope is further advanced into the nose, the next structure encountered is the
middle turbinate. The middle turbinate is a key landmark in endoscopic sinus surgery. It has a
vertical component (lying in the sagittal plane, running from posterior to anterior) and a
horizontal component (lying in the coronal plane, running from medial to lateral).

Superiorly, the middle turbinate attaches to the skull base at the cribriform plate. As such,
care should always be taken when manipulating the middle turbinate. The horizontal
component of the middle turbinate is referred to as the basal (or grand) lamella, and it
represents the dividing point between anterior and posterior ethmoid air cells. Posteriorly and
inferiorly, the middle turbinate attaches to the lateral nasal wall at the crista ethmoidalis, just
anterior to the sphenopalatine foramen.

Uncinate process

The uncinate process is the next key structure to be identified in endoscopic sinus surgery.
This L-shaped bone of the lateral nasal wall forms the anterior border of the hiatus
semilunaris, or the infundibulum. The infundibulum is the location of the ostiomeatal
complex, where the natural ostium of the maxillary sinus opens.

For patients with sinus disease, a patent ostiomeatal complex is critical for improvement
of symptoms. Anteriorly, the uncinate process attaches to the lacrimal bone, and inferiorly,
the uncinate process attaches to the ethmoidal process of the inferior turbinate.

Natural maxillary ostium

Once the uncinate process is removed, the natural maxillary ostium can be seen, typically
just posterior to the uncinate process, roughly one third of the distance along the middle
turbinate from its anterior edge. It lies at approximately the level of the inferior border of the
middle turbinate, superior to the inferior turbinate.

The natural maxillary ostium is the destination for the mucociliary flow within the
maxillary sinus. Therefore, for optimal results, the surgically enlarged maxillary antrostomy
must include the natural ostium. In fact, failure to include the maxillary ostium in endoscopic
surgical antrostomy is one of the key patterns of failure in functional endoscopic sinus

The maxillary sinus, approximately 14-15 mL in volume, is bordered superiorly by the

inferior orbital wall, medially by the lateral nasal wall, and inferiorly by the alveolar portion
of the maxillary bone.

Ethmoid bulla

The next structure to be encountered is the ethmoid bulla, which is one of the most
constant anterior ethmoidal air cells. It is just beyond the natural ostium of the maxillary
sinus and forms the posterior border of the hiatus semilunaris.

The lateral extent of the bulla is the lamina papyracea. Superiorly, the ethmoid bulla may
extend all the way to the ethmoid roof (the skull base). Alternatively, a suprabullar recess
may exist above the roof of the bulla. A careful preoperative review of the patient's CT scan
clarifies this relationship.

Ethmoid sinus

The ethmoid sinus consists of a variable number (typically 7-15) of air cells. The most
lateral border of these air cells is the lamina papyracea, and the most superior border of these
cells is the skull base. Supraorbital ethmoid cells may be present. A review of the patient's
CT scan alerts the surgeon to these variations.

The basal lamella of the middle turbinate separates the anterior ethmoid cells from the
posterior ethmoid cells. Anterior ethmoid cells drain to the middle meatus, and the posterior
cells drain into the superior meatus.

Sphenoid sinus

Exenteration of the posterior ethmoid cells exposes the face of the sphenoid. The sphenoid
sinus is the most posterior of the paranasal sinuses, sitting just superior to the nasopharynx
and just anterior and inferior to the sella turcica. The anterior face of the sphenoid sits
approximately 7 cm from the nasal sill on a 30 axis from the horizontal.

Several important structures are related to the sphenoid sinus. The internal carotid artery is
typically the most posterior and medial impression seen within the sphenoid sinus. In
approximately 7% of cases, the bone is dehiscent.

The optic nerve and its bony encasement produce an anterosuperior indentation within the
roof of the sphenoid sinus. In 4% of cases, the bone surrounding the optic nerve is dehiscent.
Therefore, controlled opening of the sphenoid sinus, typically at its natural ostium, is critical
for a safe outcome.

The location of the natural ostium of the sphenoid sinus is variable. In approximately 60%
of people, the ostium is located medial to the superior turbinate, and in 40%, it is located
lateral to the superior turbinate.

Frontal recess

The frontal recess, or the frontal sinus outflow tract, is the tract that leads from the frontal
sinus into the nasal cavity. Often, the ethmoid bulla is the posterior border of the frontal sinus
outflow tract.

Anteriorly, the frontal sinus outflow tract is bordered by the uncinate process or the agger
nasi cells (frontal anterior ethmoid air cells). If any of these cells are enlarged or if scarring is
present from a previous surgery, resultant outflow tract obstruction, leading to frontal
sinusitis, may occur. Typically, the medial wall of the frontal recess is formed by the lamina

For more information about the relevant anatomy, see Paranasal Sinus Anatomy, Nasal
Anatomy, and Skull Base Anatomy.


Anesthesia for Endoscopic Sinus Surgery

Patients may undergo functional endoscopic sinus surgery under intravenous sedation and
local anesthesia or under general anesthesia. The authors' institutional preference is general

Overview of Endoscopic Sinus Surgery

The procedure begins with decongestion of the nose and infiltration of lidocaine with
epinephrine (1% lidocaine with 1:100,000 epinephrine is used for injection). The lateral nasal
wall near the uncinate process is injected. Using a 3-mL syringe while placing a slight bend
to the 27-gauge needle facilitates the injection.

Next, the superior inlet and the anterior face of the middle turbinate are injected
submucosally. If the possibility of septoplasty exists, the septum should also be injected.
Next, 4 mL of 4% cocaine is placed onto pledgets, which are placed bilaterally in the nares. A
throat pack may be placed, or alternatively, the stomach may be suctioned prior to extubation
upon completion of the procedure.

The patient is then draped for surgery. If image-guided surgery is to be used, the
appropriate headset apparatus should be applied at this time.

Endoscopic Uncinectomy

Functional endoscopic sinus surgery may begin with uncinectomy. If the uncinate process
can be initially visualized without manipulating the middle turbinate, uncinectomy can be
performed directly. Otherwise, the middle turbinate is gently medialized, carefully using the
curved portion of the Freer elevator to avoid mucosal injury to the turbinate and to avoid
forceful medialization and fracture of the turbinate.

Next, uncinectomy may be performed via an incision with either the sharp end of the Freer
elevator or a sickle knife. The incision should be placed at the most anterior portion of the
uncinate process, which is softer on palpation in comparison to the firmer lacrimal bone,
where the nasolacrimal duct is located. Then, a Blakesley forceps is used to grasp the free
uncinate edge and to remove it.

Complete uncinectomy is important for subsequent visualization. Incomplete uncinectomy

is a common reason for failure with primary surgery. The backbiter may also be directly used
to take down the uncinate process.

Maxillary Antrostomy/Ethmoidectomy
Once the uncinate process is taken down, the true natural ostium of the maxillary sinus
should be identified. The protected eye may be palpated at this juncture to ensure that there is
no dehiscence of the lamina papyracea and to confirm the location of the lamina. The natural
ostium is typically at the level of the inferior edge of the middle turbinate about one third of
the way back.

A true cutting instrument is used to circumferentially enlarge the natural ostium. The
optimal diameter for the maxillary antrostomy is controversial; typically, a diameter of 1 cm
allows for adequate outflow and for postoperative monitoring in the office. Care should
always be taken to avoid penetrating the lamina papyracea.

Anterior Ethmoidectomy

Next, the ethmoid bulla should be identified and opened. A J-shaped curette may be used
to open the bulla at its interior and medial aspect. Once the cell is entered, the bony portions
may be carefully removed using a microdebrider or a true-cutting forceps. Complete
resection of the lateral bulla facilitates proper visualization and dissection posteriorly. Again,
care should be taken laterally to maintain an intact lamina papyracea.

The remainder of the anterior ethmoid cells may be uncapped initially with a J curette and
further opened with a microdebrider or a true cutting forceps. Using a curette initially allows
for tactile sensation and determination of the thickness of bone and verifies proper orientation
prior to further opening of cells with powered instrumentation. Care should always be taken
to avoid mucosal stripping, because mucosal preservation results in superior postoperative

Anterior ethmoid cells should be cleared to the skull base, with the surgeon exercising
caution when approaching the ethmoid roof and maintaining constant reference to the
endoscopic view and to the preoperative CT scan. Image-guided surgery or computer-aided
surgery also guides the surgeon as to the distance to the skull base, but it does not replace the
need for an intimate knowledge of the anatomy.

While moving posteriorly to new air cells, the surgeon should always enter inferiorly and
medially and then subsequently open laterally and superiorly once the more distal anatomy
can be judged by visualization and palpation. Anterior ethmoidectomy is complete upon
reaching the basal lamella of the middle turbinate.
If the sinus disease is limited to the anterior ethmoid cells and the maxillary sinus, the
procedure may end with simple anterior ethmoidectomy and maxillary antrostomy. If,
however, significant radiographic and clinical disease of the posterior ethmoid and sphenoid
is present, then dissection should continue to exenterate the posterior ethmoid cells and to
perform adequate sphenoidotomy as appropriate.

Posterior Ethmoidectomy

Posterior ethmoidectomy begins with perforating the basal lamella just superior and lateral
to the junction of the vertical and horizontal segments of the middle turbinate. Care must be
taken to preserve the posterior sagittal section of the middle turbinate and the inferior portion
of the coronal segment of the basal lamella. Preserving this L-shaped strut ensures the
stability of the middle turbinate. The lateral and superior portions of the basal lamella may
then be removed using the microdebrider.

Further posterior ethmoid cells may be taken down in a similar fashion, keeping in mind
the location of the skull base and the lamina. The surgeon must be cognizant that the skull
base typically slopes inferiorly at an approximately 30 angle from anterior to posterior.
Thus, the skull base lies lower posteriorly than anteriorly. This dissection is taken back to the
face of the sphenoid.

Enlargement of the Natural Ostium of the Sphenoid Sinus

In the absence of Onodi cells, the sphenoid ostium lies medial and posterior to the final
posterior ethmoid cell. A rough guide is that the face of the sphenoid is approximately 7 cm
from the nasal sill at a 30 angle from the horizontal. Identifying the superior turbinate aids in
the confirmation of position. The superior turbinate inserts on the anterior face of the
sphenoid sinus.

The sphenoid sinus is entered just medial and inferior to its natural ostium with a J curette
or an olive-tipped suction. Once the sinus is entered safely, the ostium can be enlarged using
a mushroom punch forceps. Care must be taken not to aggressively enter the sinus because
dehiscences may be present in the bony coverage of the carotid artery or the optic nerve.

Frontal Sinus Work

Frontal sinus work is typically reserved for the end of the surgical procedure because
manipulation may create bleeding and obscure further posterior work. If frontal sinus work is
indicated, a 45 or a 70 telescope proves useful.

Typically, an agger nasi or frontal cell is the cause of frontal outflow obstruction. Using an
angled scope for visualization, a frontal sinus curette is passed above the cell and then pulled
anteriorly, thus breaking posterior and superior cell walls.

Particular care must be exercised when working in the frontal recess, because the lamina
and the skull base sit in immediate proximity to the outflow tract. Image-guided and
navigational systems for computer-aided surgery and intimate knowledge of the anatomy are
critical for safe frontal sinus work. Kuhn and Javer provide further discussion of endoscopic
frontal sinus surgery.[8]

Nasal Packing and Spacer Placement

Once dissection is complete and hemostasis is achieved, a bacitracin-coated Telfa or Afrin

soaked pledget is placed into the nostril. Some surgeons also place Gelfilm or a dissolvable
spacer within the middle meatus to keep the space open and to prevent lateralization of the
middle turbinate and synechiae formation.


Nasal packing is removed prior to discharge of the patient. The patient is discharged with
saline nasal spray (eg, OCEAN Nasal Spray) and antibiotics, as well as instructions for a
follow-up visit in 1 week. If a spacer was placed in the middle meatus, it should be removed
or suctioned away on the first postoperative visit.

Outcome and Prognosis

Outstanding short- and long-term results have been reported for endoscopic sinus surgery.
In one study, symptoms improved in 66 of 72 patients following this surgery, with a mean
follow-up time of 7.8 years.[1] In another report, quality of life improved for 85% of the
patient population, with a mean follow-up time of 31.7 months.[2]

All risks and benefits should be candidly discussed with patients as part of the informed
consent process prior to surgery. A patient should never undergo surgery without a full
discussion of all possible complications.

Risks associated with endoscopic sinus surgery are as follows:


Synechiae formation

Orbital injury


Orbital hematoma


CSF leak

Direct brain injury

Nasolacrimal duct injury/epiphora

1. Messerklinger W. Endoscopy of the nose. Baltimore, MD: Urban & Schwarzenberg;

2. Wigand ME. Transnasal ethmoidectomy under endoscopical control. Rhinology. 1981

Mar. 19(1):7-15. [Medline].

3. Wigand ME, Steiner W, Jaumann MP. Endonasal sinus surgery with endoscopical
control: from radical operation to rehabilitation of the mucosa. Endoscopy. 1978 Nov.
10(4):255-60. [Medline].

4. Senior BA, Kennedy DW, Tanabodee J, Kroger H, Hassab M, Lanza D. Long-term

results of functional endoscopic sinus surgery. Laryngoscope. 1998 Feb. 108(2):151-
7. [Medline].

5. Damm M, Quante G, Jungehuelsing M, Stennert E. Impact of functional endoscopic

sinus surgery on symptoms and quality of life in chronic rhinosinusitis.
Laryngoscope. 2002 Feb. 112(2):310-5. [Medline].

6. Bolger WE, Brown CL, Church CA, Goldberg AN, Karanfilov B, Kuhn FA, et al.
Safety and outcomes of balloon catheter sinusotomy: a multicenter 24-week analysis
in 115 patients. Otolaryngol Head Neck Surg. 2007 Jul. 137(1):10-20. [Medline].

7. Aukema AA, Mulder PG, Fokkens WJ. Treatment of nasal polyposis and chronic
rhinosinusitis with fluticasone propionate nasal drops reduces need for sinus surgery.
J Allergy Clin Immunol. 2005 May. 115(5):1017-23. [Medline].

8. Kuhn FA, Javer AR. Primary endoscopic management of the frontal sinus.
Otolaryngol Clin North Am. 2001 Feb. 34(1):59-75. [Medline].

Fungal Sinusitis

Fungal infections of the sinuses have recently been blamed for causing most cases of chronic
rhinosinusitis. The evidence, though, is still controversial. Most fungal sinus infections are
benign or noninvasive, except when they occur in individuals who are immunocompromised.
Several reports are available that have shown invasive fungal infections in immunocompetent
individuals.[1, 2, 3]

Distinguishing invasive disease from noninvasive disease is important because the treatment
and prognosis are different for each. Noninvasive disease has 2 varieties of presentations, and
invasive disease has 3 varieties of presentations. This article reviews all 5 varieties. For
excellent patient education resources, see eMedicineHealth's Headache and Migraine Center.
Also, visit eMedicineHealth's patient education article Sinus Infection.

Axial CT scan of sinuses shows a right fungal maxillary sinusitis with an expanding mass
(possibly aspergillosis).

History of the Procedure

Fungal infections of the paranasal sinuses are uncommon and usually occur in individuals
who are immunocompromised. However, recently, the occurrence of fungal sinusitis has
increased in the immunocompetent population.

The most common pathogens are from Aspergillus and Mucor species. Aspergillosis can
cause noninvasive or invasive infections. Invasive infections are characterized by dark, thick,
greasy material found in the sinuses. Invasive infections can cause tissue invasion and
destruction of adjacent structures (eg, orbit, CNS). Noninvasive infections cause symptoms of
sinusitis, and the sinus involved is opacified on radiographic studies. Routine cultures from
the sinuses rarely demonstrate the fungus. However, the fungus is usually suspected upon
reviewing the CT scan result and is detected on removal of the secretions from the sinus.


Fungal infections of the paranasal sinus can manifest as 2 distinct entities.

The more serious infection commonly occurs in patients with diabetes or in individuals who
are immunocompromised and is characterized by its invasiveness, tissue destruction, and
rapid onset. Early detection and treatment are vital for these infections because of the high
mortality rate.

Noninvasive infections are chronic and are usually treated for extended periods as chronic
sinusitis before the condition is recognized.


Noninvasive fungal sinusitis

Two forms are described in this category: allergic fungal sinusitis and sinus mycetoma/ball.

Most commonly, Curvularia lunata,Aspergillus fumigatus, and Bipolaris and Drechslera

species cause allergic fungal sinusitis. A fumigatus and dematiaceous fungi most commonly
cause sinus mycetoma.

A study by Lu-Myers et al found that socioeconomic factors differed between patients with
allergic fungal rhinosinusitis and those with chronic rhinosinusitis, with the latter tending to
be white and older, with a higher income and greater access to primary care. The study,
which involved a total of 186 patients (93 patients in each group), also found that patients
with allergic fungal rhinosinusitis tended to have greater quantitative serum immunoglobulin
E (IgE) levels and higher Lund-Mackay scale scores than did patients with chronic

Invasive fungal sinusitis

Invasive fungal sinusitis includes the acute fulminant type, which has a high mortality rate if
not recognized early and treated aggressively, and the chronic and granulomatous types.

Saprophytic fungi of the order Mucorales, including Rhizopus, Rhizomucor, Absidia ,Mucor,
Cunninghamella, Mortierella, Saksenaea, and Apophysomyces species, cause acute invasive
fungal sinusitis. A fumigatus is the only fungus associated with chronic invasive fungal
sinusitis. Aspergillus flavus exclusively has been associated with granulomatous invasive
fungal sinusitis.


Allergic fungal sinusitis

Allergic rhinitis is prevalent in this group and is considered to be the trigger mechanism
behind allergic fungal sinusitis. Patients are immunocompetent and often have asthma,
eosinophilia, and elevated total fungus-specific IgE concentrations.[5]

Surgery reveals greenish black or brown material (ie, allergic mucin), which has the
consistency of peanut butter mixed with sand and glue. Allergic mucin and polyps may form
a partially calcified expansile mass that obstructs sinus drainage. Growth of the mass may
cause pressure-induced erosion of bone, rupture of sinus walls, and occasional leakage of the
sinus contents into the orbit or brain.

A study by Gupta et al indicated that allergic fungal rhinosinusitis tends to be more severe
when granulomas are present. The study involved 57 patients with allergic fungal
rhinosinusitis, including nine patients with granulomas, with the investigators finding that
those with granulomas had a tendency toward orbital and skull base erosion, as well as
telecanthus, diplopia, exophthalmos, and facial pain.[6]

Sinus mycetoma

This condition is usually unilateral and involves the maxillary sinus. Mucopurulent, cheesy,
or claylike material is present at the time of surgery. Patients with sinusitis mycetoma are
immunocompetent. Allergic conditions and fungus-specific IgE are less common.

Acute invasive fungal sinusitis

Acute invasive fungal sinusitis results from a rapid spread of fungi through vascular invasion
into the orbit and CNS. It is common in patients with diabetes and in patients who are
immunocompromised and has been reported in immunocompetent individuals. Typically,
patients with acute invasive sinusitis are severely ill with fever, cough, nasal discharge,
headache, and mental status changes. They usually require hospitalization.

Chronic invasive fungal sinusitis

Chronic invasive fungal sinusitis is a slowly progressive fungal infection with a low-grade
invasive process and usually occurs in patients with diabetes.

Orbital apex syndrome, which is characterized by a decrease in vision and ocular immobility
due to a mass in the superior portion of the orbit, is usually associated with this condition.

Granulomatous invasive fungal sinusitis

This condition has been reported almost exclusively in immunocompetent individuals from
North Africa. Generally, proptosis is associated with granulomatous invasive fungal sinusitis.


Allergic fungal sinusitis

Patients present with symptoms of chronic sinusitis, which may include facial pressure,
headache, nasal stuffiness, discharge, and cough. The condition should be suspected in
individuals with intractable sinusitis and nasal polyposis.

Some patients may present with proptosis or eye muscle entrapment. These patients usually
have atopy and have had multiple surgeries by the time of diagnosis. CT scanning of the
sinuses reveals opacification with concretions and/or calcifications.

Sinus mycetoma

Presentation of patients with sinus mycetoma is similar to that of patients with sinusitis.
Examination may reveal polyposis with evidence of sinusitis, mainly on one side. The main
report is blowing of gravel-like material from the nose. Usually, sinus mycetoma is found
accidentally on CT scanning of the sinuses.

Acute invasive fungal sinusitis

Patients are usually hospitalized and are very sick with fever, cough, nasal discharge,
headache, and mental status changes. A high index of suspicion for early diagnosis is critical,
especially in individuals who are immunocompromised.

Signs and symptoms include dark ulcers on the septum, turbinates, or palate. In the late
stages, signs and symptoms of cavernous sinus thrombosis are present.

Chronic invasive fungal sinusitis

Patients present with symptoms of long-standing sinusitis. Symptoms are usually not acute,
and fever and mental status changes are absent.

Orbital apex syndrome, which is characterized by a decrease in vision and ocular immobility
due to a mass in the superior portion of the orbit, is usually associated with this condition.

Nasal examination findings can be minimal. However, findings from the eye examination can
be positive.

Granulomatous invasive fungal sinusitis

Patients present with symptoms of chronic sinusitis associated with proptosis. Examination of
the nasal cavity can be nonrevealing. However, findings from the eye examination are usually


The treatment of choice for all types of fungal sinusitis is surgical (see Surgical therapy).

Relevant Anatomy

See Surgical therapy.


All forms of fungal sinusitis require surgical treatment. The only contraindications to surgical
management relate to the general condition of the patient. Before surgery is recommended,
risks and benefits of the surgical procedure should be weighed against the risks of general
Laboratory Studies

See the list below:

Elevated total fungus-specific IgE concentrations are often found in patients with
allergic fungal sinusitis. This is less common in patients with sinus mycetoma.

Using enzyme-linked immunosorbent assays, one study examined the sinonasal tissue
and secretions in patients with chronic rhinosinusitis for the presence of mycotoxins
(ie, aflatoxin, deoxynivalenol, zearalenone, ochratoxin, and fumonisin) to determine
their possible role, if any, in chronic rhinosinusitis. No mycotoxins were found,
except ochratoxin in 4 of 18 samples. The clinical significance of these results has not
been determined. [7]

Middlebrooks et al devised a seven-variable, computed tomography (CT) scanbased

diagnostic model for acute invasive fungal rhinosinusitis. They reported that an abnormality
associated with one of the models variableswhich consist of periantral fat, bone
dehiscence, orbital invasion, septal ulceration, the pterygopalatine fossa, the nasolacrimal
duct, and the lacrimal sachas a positive predictive value of 87%, a negative predictive
value of 95%, a sensitivity of 95%, and a specificity of 86%, while the involvement of two
variables gives the model a specificity of 100% and a positive predictive value of 100%.[8]

Imaging Studies

See the list below:

CT scanning of the paranasal sinuses in the coronal views is essential in the

evaluation of patients in whom fungal sinusitis is suspected. [9, 10]

MRI with enhancement may be helpful in assessing patients with allergic fungal
sinusitis and in patients in whom invasive fungal sinusitis is suspected. [10]

o MRI may show low signal intensity, suggesting a fungal process versus a solid
mass in allergic fungal sinusitis.

o MRI is helpful in evaluating CNS spread in invasive fungal sinusitis.

Histologic Findings
In allergic fungal sinusitis, allergic mucin contains intact and degenerated eosinophils,
Charcot-Leyden crystals, cellular debris, and sparse hyphae. The sinus mucosa has mixed
cellular infiltrate of eosinophils, plasma cells, and lymphocytes. The mucus membrane is not
invaded by fungi.

No allergic mucin is present in sinus mycetoma. However, the sinus contains dense material
that consists of hyphae separate from but adjacent to the mucosa. The sinus mucosa is not

Histopathologic studies in acute invasive fungal sinusitis reveal hyphal invasion of the
mucosa, submucosa, and blood vessels, including the carotid arteries and cavernous sinuses;
vasculitis with thrombosis; hemorrhage; and tissue infarction.

Necrosis of the mucosa, submucosa, and blood vessels, with low-grade inflammation, is
observed in chronic invasive fungal sinusitis.

Granuloma with multinucleated giant cells with pressure necrosis and erosion is observed in
granulomatous invasive fungal sinusitis.

Treatment & Management

Medical Therapy

The treatment of choice for all types of fungal sinusitis is surgical. Medical treatment
depends on the type of infection and the presence of invasion.

Allergic fungal sinusitis

The treatment of choice is generally surgery. Systemic steroids may be indicated once
surgery is performed and the diagnosis is confirmed. Some authors suggest a low dose of
prednisone (0.5 mg/kg) in a tapering dose with alternate-day dosage over a 3-month period.
Topical nasal steroids are helpful postoperatively. Aggressive nasal salt-water washes are
recommended. Immune therapy for specific allergens is controversial, even though some
reports suggest benefit from this treatment. Systemic antifungals are not indicated in the
absence of invasion.

Sinus mycetoma
The recommended treatment is surgical. Once the fungus ball is removed, no further medical
treatment is indicated, except for the underlying condition. No antifungal treatment is

Chronic invasive fungal sinusitis

Surgical treatment is mandatory. Initiate medical treatment with systemic antifungals once
invasion is diagnosed. Amphotericin B (2 g/d) is recommended; this can be replaced by
ketoconazole or itraconazole once the disease is under control.

A study by Mehta et al suggested that itraconazole may be as effective as amphotericin B in

the treatment of chronic invasive fungal sinusitis. In a prospective, randomized, unblinded
study of 26 immunocompetent patients, one group (10 patients) was treated with
amphotericin B and the other (16 patients) with itraconazole. A complete cure was achieved
in two patients in the amphotericin-B group and five in the itraconazole group, while four
amphotericin-B patients and seven itraconazole patients experienced persistent disease, and
one amphotericin-B patient and three itraconazole patients had relapses. In addition, three
patients died, and one was lost to follow-up. Based on relative risk analysis, the investigators
concluded that itraconazole and amphotericin B worked equally well against chronic invasive
fungal sinusitis.[11]

Acute invasive fungal sinusitis

Emergent treatment is necessary once this condition is suspected. Initiate systemic antifungal
treatment after surgical debridement. High doses of amphotericin B (1-1.5 mg/kg/d) are
recommended. Oral itraconazole (400 mg/d) can replace amphotericin B once the acute stage
has passed. Treatment of the underlying immune deficiency, if possible, is desirable.

Chronic granulomatous fungal sinusitis

Surgical debridement is the mainstay of treatment, followed by systemic antifungal

medications. Recurrence of this condition is rare.

Surgical Therapy

Allergic fungal sinusitis

Surgery is generally considered the treatment of choice. Goals of surgical therapy are
conservative debridement of the allergic mucin and polyps (if present) from the involved
sinuses and restoration of sinus aeration. Goals may be achieved endoscopically if possible.
An external approach can be considered if the lesion is not accessible endoscopically.
Adequate ventilation of the sinus is essential to prevent relapse or recurrence of the disease
once the disease is exenterated.

Sinus mycetoma

Surgical removal of the fungus ball with aeration of the sinus is the only requirement. Once
this is accomplished, no further medical treatment is indicated, except for the underlying
condition. Endoscopic lesion removal can be performed when the lesion is accessible.
Consider an external approach in patients in whom the mycetoma cannot be removed

Acute invasive fungal sinusitis

Perform emergency surgery once this condition is suspected. Perform radical debridement of
the necrotic tissue until normal tissue is reached. Often, debridement is achieved via external
approaches. In some cases, the skull-base team should be involved.

Chronic invasive fungal sinusitis

This condition is usually less aggressive than the acute stage. Surgical debridement is still
warranted and can be approached endoscopically in some patients. Consider an external
approach when adequate debridement cannot be achieved endoscopically.

Chronic granulomatous fungal sinusitis

Surgical debridement is the treatment of choice. Endoscopic and external approaches can be


Allergic fungal sinusitis

Long-term follow-up care is required for maintenance of the sinus cavities; this may be
achieved via endoscopic examination and debridement in the office. A short course of
systemic steroids may be readministered if any signs of relapse or recurrence are seen.
Surgical debridement may be necessary if systemic steroids fail to control the disease.

Sinus mycetoma
Long-term follow-up care is not required once the lesions are healed and patency of the
sinuses is maintained.

Acute invasive fungal sinusitis

This condition is rare and is usually associated with a high mortality rate. Survivors may have
facial deformities and require long-term follow-up care by several specialists, including head
and neck surgeons, infectious-disease specialists, and immunodeficiency specialists.

Chronic invasive fungal sinusitis

This condition tends to recur. Therefore, long-term follow-up care is recommended.

Chronic granulomatous fungal sinusitis

Experience with this condition is limited. Prognosis is good, but a tendency toward
recurrence exists.


Allergic fungal sinusitis

Erosion into the adjacent structures may occur if the condition is left untreated. Erosion is
most often observed in individuals who present with proptosis. Sinusitis symptoms worsen
and do not respond to routine antimicrobial therapy.

Sinus mycetoma

Fungus balls, if left untreated, cause worsening of sinusitis symptoms, with the potential for
complicated sinusitis. This may predispose the patient to complications, such as those
involving the orbit and CNS.

Acute invasive fungal sinusitis

Initiate emergency treatment once this condition is suspected. This is a rapidly progressive
disease that invades adjacent structures, causing tissue damage and necrosis. Cavernous sinus
thrombosis and invasion of the CNS are common and carry a mortality rate of 50-80%.

Chronic invasive fungal sinusitis

Invasion into adjacent structures is not as common as in the acute type. However, erosion into
the orbit or CNS is likely if the disease is left untreated.

Chronic granulomatous fungal sinusitis

Erosion into the adjacent structures (eg, orbit, CNS) is likely. Initiate aggressive therapy to
avoid erosion.

Outcome and Prognosis

Allergic fungal sinusitis

This disorder carries a good prognosis following adequate surgical debridement and aeration
of the sinuses. Close follow-up care is important. Long-term use of topical steroids controls
relapses. Short-term systemic steroids may be required when relapses occur.

Sinus mycetoma

This condition has an excellent prognosis once the fungus ball is removed and adequate
aeration of the sinus is restored. No long-term follow-up care is required for most patients.

Acute invasive fungal sinusitis

This condition carries a poor prognosis. Mortality rate is reported at 50%, even with
aggressive surgical and medical treatment. Relapses are common during subsequent episodes
of neutropenia. Treatment with systemic antifungals as prophylaxis is indicated in cases of

Chronic invasive fungal sinusitis

Good prognosis has been noted in patients who receive a prolonged course of systemic
antifungals. Patients who receive shorter courses of systemic antifungals have more relapses,
thereby requiring further treatment.

Chronic granulomatous fungal sinusitis

Experience with this condition is limited. Generally, prognosis is good, but a tendency toward
recurrence exists.

1. Hussain S, Salahuddin N, Ahmad I, Salahuddin I, Jooma R. Rhinocerebral invasive

mycosis: occurrence in immunocompetent individuals. Eur J Radiol. 1995 Jul.
20(2):151-5. [Medline].

2. Scharf JL, Soliman AM. Chronic rhizopus invasive fungal rhinosinusitis in an

immunocompetent host. Laryngoscope. 2004 Sep. 114(9):1533-5. [Medline].

3. Siddiqui AA, Shah AA, Bashir SH. Craniocerebral aspergillosis of sinonasal origin in
immunocompetent patients: clinical spectrum and outcome in 25 cases. Neurosurgery.
2004 Sep. 55(3):602-11; discussion 611-3. [Medline].

4. Lu-Myers Y, Deal AM, Miller JD, et al. Comparison of Socioeconomic and

Demographic Factors in Patients with Chronic Rhinosinusitis and Allergic Fungal
Rhinosinusitis. Otolaryngol Head Neck Surg. 2015 Apr 27. [Medline].

5. Pant H, Schembri MA, Wormald PJ, Macardle PJ. IgE-mediated fungal allergy in
allergic fungal sinusitis. Laryngoscope. 2009 Apr 8. [Medline].

6. Gupta R, Gupta AK, Patro SK, et al. Allergic fungal rhino sinusitis with granulomas:
A new entity?. Med Mycol. 2015 May 30. [Medline].

7. Lieberman SM, Jacobs JB, Lebowitz RA, Fitzgerald MB, Crawford J, Feigenbaum
BA. Measurement of Mycotoxins in Patients with Chronic Rhinosinusitis.
Otolaryngol Head Neck Surg. 2011 Mar 31. [Medline].

8. Middlebrooks EH, Frost CJ, De Jesus RO, Massini TC, Schmalfuss IM, Mancuso
AA. Acute Invasive Fungal Rhinosinusitis: A Comprehensive Update of CT Findings
and Design of an Effective Diagnostic Imaging Model. AJNR Am J Neuroradiol. 2015
Apr 16. [Medline].

9. Gamba JL, Woodruff WW, Djang WT, Yeates AE. Craniofacial mucormycosis:
assessment with CT. Radiology. 1986 Jul. 160(1):207-12. [Medline].

10. Manning SC, Merkel M, Kriesel K, Vuitch F, Marple B. Computed tomography and
magnetic resonance diagnosis of allergic fungal sinusitis. Laryngoscope. 1997 Feb.
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11. Mehta R, Panda NK, Mohindra S, et al. Comparison of efficacy of amphotericin B
and itraconazole in chronic invasive fungal sinusitis. Indian J Otolaryngol Head Neck
Surg. 2013 Aug. 65:288-94. [Medline]. [Full Text].

12. Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of
rhinitis: an updated practice parameter. J Allergy Clin Immunol. 2008 Aug. 122(2
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13. Anselmo-Lima WT, Lopes RP, Valera FC, Demarco RC. Invasive fungal
rhinosinusitis in immunocompromised patients. Rhinology. 2004 Sep. 42(3):141-4.

14. Corey JP, Romberger CF, Shaw GY. Fungal diseases of the sinuses. Otolaryngol
Head Neck Surg. 1990 Dec. 103(6):1012-5. [Medline].

15. deShazo RD. Fungal sinusitis. Am J Med Sci. 1998 Jul. 316(1):39-45. [Medline].

16. deShazo RD, O'Brien M, Chapin K, Soto-Aguilar M, Gardner L, Swain R. A new

classification and diagnostic criteria for invasive fungal sinusitis. Arch Otolaryngol
Head Neck Surg. 1997 Nov. 123(11):1181-8. [Medline].

17. Gillespie MB, O'Malley BW Jr, Francis HW. An approach to fulminant invasive
fungal rhinosinusitis in the immunocompromised host. Arch Otolaryngol Head Neck
Surg. 1998 May. 124(5):520-6. [Medline].

18. Gosepath J, Mann WJ. Role of fungus in eosinophilic sinusitis. Curr Opin
Otolaryngol Head Neck Surg. 2005 Feb. 13(1):9-13. [Medline].

19. Jahrsdoerfer RA, Ejercito VS, Johns MM, Cantrell RW, Sydnor JB. Aspergillosis of
the nose and paranasal sinuses. Am J Otolaryngol. 1979 Fall. 1(1):6-14. [Medline].

20. Lansford BK, Bower CM, Seibert RW. Invasive fungal sinusitis in the
immunocompromised pediatric patient. Ear Nose Throat J. 1995 Aug. 74(8):566-73.

21. Ochi JW, Harris JP, Feldman JI, Press GA. Rhinocerebral mucormycosis: results of
aggressive surgical debridement and amphotericin B. Laryngoscope. 1988 Dec.
98(12):1339-42. [Medline].
22. Press GA, Weindling SM, Hesselink JR, Ochi JW, Harris JP. Rhinocerebral
mucormycosis: MR manifestations. J Comput Assist Tomogr. 1988 Sep-Oct.
12(5):744-9. [Medline].

23. Sasama J, Sherris DA, Shin SH, Kephart GM, Kern EB, Ponikau JU. New paradigm
for the roles of fungi and eosinophils in chronic rhinosinusitis. Curr Opin Otolaryngol
Head Neck Surg. 2005 Feb. 13(1):2-8. [Medline].

24. Schubert MS, Hutcheson PS, Graff RJ, Santiago L, Slavin RG. HLA-DQB1 *03 in
allergic fungal sinusitis and other chronic hypertrophic rhinosinusitis disorders. J
Allergy Clin Immunol. 2004 Dec. 114(6):1376-83. [Medline].

25. Shin SH, Ponikau JU, Sherris DA, et al. Chronic rhinosinusitis: an enhanced immune
response to ubiquitous airborne fungi. J Allergy Clin Immunol. 2004 Dec.
114(6):1369-75. [Medline].

26. Sohail MA, Al Khabori MJ, Hyder J, Verma A. Allergic fungal sinusitis: can we
predict the recurrence?. Otolaryngol Head Neck Surg. 2004 Nov. 131(5):704-10.

27. Washburn RG. Fungal sinusitis. Curr Clin Top Infect Dis. 1998. 18:60-74. [Medline].

28. Wise SK, Venkatraman G, Wise JC, DelGaudio JM. Ethnic and gender differences in
bone erosion in allergic fungal sinusitis. Am J Rhinol. 2004 Nov-Dec. 18(6):397-404.
Medical Treatment for Acute Sinusitis


Many classifications, both clinical and radiological, have been proposed in the literature to
define acute sinusitis. Although no consensus on the precise definition currently exists, acute
sinusitis may be defined as a bacterial or viral infection of the sinuses of fewer than 4 weeks
duration that resolves completely with appropriate treatment. Subacute sinusitis represents a
temporal progression of symptoms for 4-12 weeks. Recurrent acute sinusitis is diagnosed
when 2-4 episodes of infection occur per year with at least 8 weeks between episodes, and, as
in acute sinusitis, the sinus mucosa completely normalizes between attacks. Chronic sinusitis
is the persistence of insidious symptomatology beyond 12 weeks, with or without acute
exacerbations, and is discussed in Sinusitis, Chronic, Medical Treatment.

Air-fluid level (arrow) in the maxillary sinus suggests sinusitis.


To properly diagnose and treat infectious disorders of the paranasal sinuses, the clinician
should have knowledge of the developmental milestones. The development of the paranasal
sinuses begins in the third week of gestation and continues until early adulthood.
During the third week of embryonic development, proliferation and medial migration of
ectodermal cells form the notochord. After the heart tube and pericardium have rotated from
the cranial position to lie anteriorly, the notochord, which is initially in the caudal region of
the embryonic disc, rotates to lie posterior to the primitive foregut. The paraxial layer of
mesenchyme, which lies adjacent to the notochord, differentiates into the somite ridges,
intermediate cell mass, and lateral plate mesoderm. From these mesodermal structures the
branchial arches develop, the first of which gives rise to internal nasal structures.

The paranasal sinuses develop in conjunction with the palate from changes in the lateral wall
of the nasal cavity. At 40 weeks' gestation, 2 horizontal grooves develop in the mesenchyme
of the lateral wall of the nasal cavity. Proliferation of maxilloturbinate mesenchyme between
these grooves results in an outpouching of tissue medially into the nasal lumen. This
outpouching is the precursor of the middle and inferior meatus as well as the inferior
turbinate. Ethmoidoturbinate folds develop superiorly to give rise to the middle and superior
turbinates. Once the turbinate structures are established, sinus development begins and
continues until early adult life.


The paranasal sinuses are air-filled bony cavities that extend from the skull base to the
alveolar process and laterally from the nasal cavity to the inferomedial aspect of the orbit and
the zygoma. They are lined with pseudostratified columnar epithelium that is contiguous, via
ostia, with the lining of the nasal cavity. This epithelium contains a number of mucous-
producing goblet cells. The arterial supply of the paranasal sinuses is from branches of the
internal and external carotid arteries, while the venous and lymphatic drainage path is through
the sinus ostia into the nasal cavity plexus. In addition, venous drainage occurs through
valveless vessels corresponding to the arterial supply. The focal point of sinus drainage is the
ostiomeatal complex, which is located in the middle meatus and is composed of the
maxillary, frontal, and anterior ethmoid ostia. The posterior ethmoids empty into the superior
meatus, and the sphenoids empty into the sphenoethmoidal recess.

The exact function of the paranasal sinuses is not well understood. The possible roles of the
sinuses may include reducing the weight of the skull; dampening pressure; humidifying and
warming inspired air; absorbing heat and insulating the brain; aiding in sound resonance;
providing mechanical rigidity; and increasing the olfactory surface area.
The sinus mucosa has less secretory and vasomotor function than the nasal cavity does. Cilia
are concentrated near and beat toward the natural sinus ostia. Blockage of the ostium results
in stasis of mucous flow, which can lead to development of disease.


The sinuses are normally sterile under physiologic conditions. Purulent sinusitis can occur
when ciliary clearance of sinus secretions decreases or when the sinus ostium becomes
obstructed, which leads to retention of secretions, negative sinus pressure, and reduction of
oxygen partial pressure. This environment is then suitable for growth of pathogenic
organisms. Factors that predispose the sinuses to obstruction and decreased ciliary function
are allergic, nonallergic, or viral insults, which produce inflammation of the nasal and sinus
mucosa and result in ciliary dysmotility and sinus obstruction. Approximately 90% of
patients who have viral upper respiratory tract infections (URTIs) have sinus involvement,
but only 5-10% of these patients have bacterial superinfection requiring antimicrobial

Anatomical variations that narrow the ostiomeatal complex, including septal deviation,
paradoxical middle turbinates, and Haller cells, make this area more sensitive to obstruction
from mucosal inflammation. Mechanical obstruction of the ostiomeatal complex from foreign
bodies, polyps, or tumors can also result in acute sinus disease. Systemic diseases that result
in decreased mucociliary clearance, including cystic fibrosis and Kartagener syndrome, can
be predisposing factors for acute sinusitis in rare cases. Patients with immunodeficiencies (eg,
agammaglobulinemia, combined variable immunodeficiency, and immunodeficiency with
reduced immunoglobulin G [IgG] and immunoglobulin A [IgA]bearing cells) are also at
increased risk of developing acute sinusitis.

Acute sinusitis in the intensive care population is a distinct entity, occurring in 18-32% of
patients with prolonged periods of intubation, and is usually diagnosed during the evaluation
of unexplained fever. Cases in which the cause is obstruction are usually evident and can
include the presence of prolonged nasogastric or nasotracheal intubation. Moreover, patients
in an intensive care setting are generally debilitated, predisposing them to septic
complications, including sinusitis.

Ciliary function is also reduced in the presence of low pH, anoxia, bacterial toxins, smoking,
dehydration, foreign bodies, and drugs (eg, atropine, antihistamines, phenylephedrine).
Approximately 10% of cases of acute sinusitis result from direct inoculation of the sinus with
a large amount of bacteria. Dental abscesses or procedures that result in communication
between the oral cavity and sinus can produce sinusitis by this mechanism. Facial trauma or
large inoculations from swimming can produce sinusitis as well.



United States

Sinusitis affects 1 out of every 7 adults in the United States, with over 30 million individuals
diagnosed each year. Acute bacterial sinusitis is the fifth most common diagnosis prompting
antibiotic administration and accounts for 0.4% of ambulatory diagnoses.[1] The economic
burden of acute sinusitis in children is $1.77 billion per year.[2]

Clinical Presentation


Acute sinusitis is a clinical diagnosis; thus, an understanding of its presentation is of

paramount importance in differentiating this entity from allergic or vasomotor rhinitis and
common URTIs. No specific clinical symptom or sign is sensitive or specific for acute
sinusitis, so the overall clinical impression should be used to guide management.

A consensus statement published in Otolaryngology-Head and Neck Surgery made strong

recommendations that clinicians should distinguish between acute rhinosinusitis caused by
bacterial causes and those episodes caused viral upper respiratory infections and
noninfectious conditions.[3] The panel suggests that the diagnosis of acute bacterial sinusitis
be entertained when (a) symptoms or signs of acute rhinosinusitis are present 10 days or more
beyond the onset of upper respiratory symptoms, or (b) symptoms or signs of acute
rhinosinusitis worsen within 10 days after an initial improvement. A history of purulent
secretions and facial or dental pain are specific symptoms that may point to a bacterial
etiology. In a patient in intensive care, acute sinusitis should be suspected in the presence of
sepsis of unknown origin.

Anterior rhinoscopic examination, with or without a topical decongestant, is important to
assess the status of the nasal mucosa and the presence and color of nasal discharge.
Predisposing anatomical variations can also be noted during anterior rhinoscopy. Sinus
transillumination and palpation are of little predictive value. A basic evaluation of ocular and
neurological function is also necessary in order to rule out potential complications.

Endoscopic examination may reveal the origin of the purulent discharge from the middle
meatus and may provide information about the nature of ostiomeatal obstruction. The use of
endoscopy may also aid in the etiologic diagnosis of acute sinusitis by allowing the careful
attainment of purulent secretions from the sinus ostia for culture.


The bacteria most commonly involved in acute sinusitis are part of the normal nasal flora.
These bacteria can become sinus pathogens when they are deposited into the sinuses by
sneezing, coughing, or direct invasion under conditions that optimize their growth. The most
common bacterial pathogens in acute sinusitis are Streptococcus pneumoniae (30-40%),
Haemophilus influenzae (20-30%), and Moraxella catarrhalis (12-20%). Staphylococcus
aureus and Streptococcus pyogenes are isolated in rare cases. Sixty-six percent of patients
with acute sinusitis grow at least 1 pathogenic bacterial species on sinus aspirates, while 26-
30% percent of patients have multiple predominant bacterial species.

Anaerobic organisms have been found in fewer than 10% of patients with acute bacterial
sinusitis, despite the ample environment available for their growth. The exceptions are in
sinusitis resulting from a dental source and in patients with chronic sinus disease, in whom
anaerobic organisms are usually isolated.

Gram-negative organisms, including Pseudomonas aeruginosa (15.9%), Escherichia coli

(7.6%), Proteus mirabilis (7.2%), Klebsiella pneumoniae, and Enterobacter species,
predominate in nosocomial sinusitis, accounting for 60% of cases. Polymicrobial invasion is
seen in 25-100% of cultures. The other pathogenic organisms found in nosocomial patients
are gram-positive organisms (31%) and fungi (8.5%). Viruses are the most common trigger
of acute sinusitis. Rhinovirus, influenza, and parainfluenza viruses are the primary pathogens
in 3-15% of patients with acute sinusitis.

Fungal causes of sinusitis are discussed in Allergic Fungal Sinusitis and Sinusitis, Fungal.
Differential Diagnoses

Acute Frontal Sinusitis Surgery

Allergic Fungal Sinusitis

Chronic Sinusitis

Fungal Sinusitis

Surgical Treatment of Acute Ethmoid Sinusitis

Surgical Treatment of Acute Maxillary Sinusitis

Surgical Treatment of Acute Sphenoid Sinusitis

Surgical Treatment of Chronic Maxillary Sinusitis


Laboratory Studies

Some authors have reported on the use of laboratory tests including sedimentation rate, white
blood cell counts, and C-reactive protein levels to help diagnose acute sinusitis.[4] These tests
appear to add little to the predictive value of clinical findings in the diagnosis.

Cultures are not routinely obtained in the evaluation of acute sinusitis but should be obtained
in a patient in intensive care or with immunocompromise, in children not responding to
appropriate medical management, and in patients with complications of sinusitis. Because the
nose is colonized with multiple nonpathogenic species of bacteria, care must be taken when
evaluating culture results. A specific organism is considered pathogenic when more than 104
colony-forming units of the species are grown on culture or when polymorph counts are
greater than 5000 cells/mL.

Imaging Studies

Imaging studies are not necessary when the probability of sinusitis is either high or low but
may be useful when the diagnosis is in doubt, based upon a thorough history and physical
examination. Plain sinus radiographs may demonstrate mucosal thickening, air-fluid levels,
and sinus opacification. Limitations of plain films include interobserver variability, inability
to distinguish infection from a polyp or tumor disease, and poor depiction of the ethmoid and
sphenoid sinuses.

CT scanning has poor specificity for the diagnosis of acute sinusitis, demonstrating sinus air-
fluid levels in 87% of individuals with simple URTIs and 40% of asymptomatic individuals.
CT scanning is the modality of choice, however, in specific circumstances such as in the
evaluation of a patient in intensive care, when complications are suspected, or in the
preoperative evaluation of surgical candidates. CT scanning can give valuable information
regarding the anatomical and mechanical contributions in the development of acute sinusitis.
Coronal views with bone windows are the preferred sinus study for evaluating each of the
sinuses as well as the ostiomeatal complex.

Magnetic resonance imaging (MRI) is excellent for evaluating soft tissue disease within the
sinuses, but it is of little value in the diagnostic workup for acute sinusitis.

Treatment & Management

Medical Care

The primary goals of management of acute sinusitis are to eradicate the infection, decrease
the severity and duration of symptoms, and prevent complications. Most patients with acute
sinusitis are treated in the primary care setting. Further evaluation by an otolaryngologist is
recommended when (1) continued deterioration occurs with appropriate antibiotic therapy,
(2) episodes of sinusitis recur, (3) symptoms persist after 2 courses of antibiotic therapy, or
(4) comorbid immunodeficiency, nosocomial infection, or complications of sinusitis are
present. The goals of management of acute sinusitis are the provision of adequate drainage
and appropriate systemic treatment of the likely bacterial pathogens.

The Joint Task Force on Practice Parameters for Allergy and Immunology suggests assessing
response to symptoms after 3-5 days of therapy and continuing for an additional 7 days if
there is improvement. Combining an intranasal corticosteroid with an antibiotic reduces
symptoms more effectively than antibiotics alone.[5]

Drainage of the involved sinus can be achieved both medically and surgically (see the
Medication and Surgical Care sections). Aggressively treat patients in intensive care who
develop acute sinusitis in order to avoid septic complications. Consider removal of
nasotracheal and nasogastric tubes and promote drainage either medically or surgically.
A retrospective cohort study by Pynnonen et al, conducted at a single academic institution,
suggested that antibiotics are being overused in the treatment of patients with mild acute
sinusitis of short duration. The investigators found that 66% of such patients were being
given antibiotics, with antibiotic use varying according to the individual provider, the
providers specialty (with emergency medicine providers tending to use more antibiotics),
and whether a medical trainee was present.[6]


A clinical practice guideline update from the American Academy of Otolaryngology-Head

and Neck Surgery provides new recommendations for clinicians on the diagnosis and
treatment of adult rhinosinusitis. Among those pertaining to acute rhinosinusitis are
recommendations that clinicians distinguish acute bacterial rhinosinusitis from acute
rhinosinusitis resulting from viral upper respiratory infections and noninfectious conditions.
It is also recommended that clinicians do the following[7] :

Offer watchful waiting (without antibiotics) or prescribe initial antibiotic therapy for
adults with uncomplicated acute bacterial rhinosinusitis

Prescribe amoxicillin with or without clavulanate as rst-line therapy for 5-10 days in
most adults if acute bacterial rhinosinusitis is being treated with an antibiotic

Reassess the patient to confirm acute bacterial rhinosinusitis, exclude other causes of
illness, and detect complications if the patient worsens or fails to improve with the
initial management option by 7 days after diagnosis or worsens during the initial
management; if acute bacterial rhinosinusitis is confirmed in a patient being managed
with observation, antibiotic therapy should commence; if the patient is already being
managed with an antibiotic, the antibiotic should be changed

Distinguish chronic rhinosinusitis and recurrent acute rhinosinusitis from isolated

episodes of acute bacterial rhinosinusitis and other causes of sinonasal symptoms

Assess the patient with chronic rhinosinusitis or recurrent acute rhinosinusitis for
multiple chronic conditions that would modify management, such as asthma, cystic
fibrosis, immunocompromised state, and ciliary dyskinesia

Surgical Care
Sinus puncture and irrigation techniques allow for a surgical means of removal of thick
purulent sinus secretions. The purpose of surgical drainage is to enhance mucociliary flow
and provide material for culture and sensitivity. A surgical means of sinus drainage should be
used when appropriate medical therapy has failed to control the infection and prolonged or
slowly resolving symptoms result or when complications of sinusitis occur. Another
indication for sinus puncture is to obtain culture material to guide antibiotic selection if
empiric therapy has failed or antibiotic choice is limited. This is particularly important in
patients who are immunocompromised or in intensive care. Sinusitis can be a prominent
source of sepsis in these patients. In adults, sinus puncture can usually be achieved using
local anesthesia; however, in children, a general anesthetic is usually necessary.

In today's era of minimally invasive surgical techniques, sinus endoscopy is commonly used
to achieve sinus drainage. It offers the advantages of (1) being able to open multiple sinuses
or to decompress the orbit in cases of complications and (2) allowing the surgeon to open the
natural ostia of the involved sinuses.

The techniques and complications of open and endoscopic sinus surgical approaches are
discussed in articles dealing with their individual surgical management.

A study by Patel et al suggested that after complicated acute pediatric sinusitis resolves
following initial medical or surgical intervention, few patients require subsequent surgical
treatment. The investigators reviewed the records of 86 children and adolescents, aged 2
months to 18 years, with either orbital (80 patients) or intracranial (6 patients) complications
of acute sinusitis; the children were treated either surgically (27 patients) or medically (59
patients) during the acute phase of the disease. The study determined that four of the patients
treated surgically and five of those treated medically needed surgery following the initial
resolution of their sinusitis; eight of the nine patients required it because medical therapy
failed for persistent rhinosinusitis, and one needed it after a second complication developed.[8]


Ophthalmological or neurosurgical consultation should be obtained when either orbital or

intracranial complications develop.


Medication Summary
Medical drainage is achieved with topical and systemic vasoconstrictors. Oral alpha-
adrenergic vasoconstrictors, including pseudoephedrine and phenylephrine, can be used for
10-14 days to allow for restoration of normal mucociliary function and drainage. Because
oral alpha-adrenergic vasoconstrictors may cause hypertension and tachycardia, they may be
contraindicated in patients with cardiovascular disease. Oral alpha-adrenergic
vasoconstrictors may also be contraindicated in competitive athletes because of rules of
competition. Topical vasoconstrictors (eg, oxymetazoline hydrochloride) provide good
drainage, but they should be used only for a maximum of 3-5 days, given the increased risk
of rebound congestion, vasodilatation, and rhinitis medicamentosa when used for longer

Mucolytic agents (eg, guaifenesin, saline lavage) have the theoretical benefit of thinning
mucous secretions and improving drainage. They are not, however, commonly used in
clinical practice in the treatment of acute sinusitis. Intranasal steroids have not been
conclusively shown to be of benefit in cases of acute sinusitis.

Antihistamines are beneficial for reducing ostiomeatal obstruction in patients with allergies
and acute sinusitis; however, they are not recommended for routine use for patients with
acute sinusitis. Antihistamines may complicate drainage by thickening and pooling sinonasal

In cases of suspected or documented bacterial sinusitis, the second principle of treatment is to

provide adequate systemic treatment of the likely bacterial pathogens (ie, S pneumoniae, H
influenzae, M catarrhalis). The physician should be aware of the probability of bacterial
resistance within their community. Approximately 44 % of H influenzae and almost all of M
catarrhalis strains have beta-lactamasemediated resistance to penicillin-based
antimicrobials in children. As many as 64% of S pneumoniae strains are penicillin resistant
because of altered penicillin-binding proteins. Multiple drugresistant S pneumoniae strains
are also found in substantial numbers of children in daycare settings.[9]

Initial selection of the appropriate antibiotic therapy should be based on the likely causative
organisms given the clinical scenario and the probability of resistant strains within a
community. The course of treatment is usually 14 days. First-line therapy at most centers is
usually amoxicillin or a macrolide antibiotic in patients allergic to penicillin because of the
low cost, ease of administration, and low toxicity of these agents. Amoxicillin should be
given at double the usual dose (80-90 mg/kg/d), especially in areas with known S
pneumoniae resistance.

Table 1. Dosage, Route, and Spectrum of Activity of Commonly Used First-Line


Antibiotic Dosa Streptococcus pneumoniae Haemophil Moraxell Anaerob

ge Sensiti Intermedi Resista us a ic
ve ate nt influenzae catarrha bacteria
Amoxicillin 500 +++ ++ + ++ + +
PO tid
Clarithromy 250- ++ ++ + ++ +++ +
cin 500
Azithromyci 500 ++ ++ + ++ +++ +
n mg
for 4
*+, low activity against microorganism; ++, moderate activity against microorganism; +++,
good activity against microorganism

Patients who live in communities with a high incidence of resistant organisms, those who fail
to respond within 48-72 hours of commencement of therapy, and those with persistence of
symptoms beyond 10-14 days should be considered for second-line antibiotic therapy. The
most commonly used second-line therapies include amoxicillin clavulanate, second- or third-
generation cephalosporins (eg, cefuroxime, cefpodoxime, cefdinir), macrolides (ie,
clarithromycin), fluoroquinolones (eg, ciprofloxacin, levofloxacin, moxifloxacin), and

In patients with dental causes of sinusitis or those with foul-smelling discharge, anaerobic
coverage using clindamycin or amoxicillin with metronidazole is necessary.

Table 2. Dosage, Route, and Spectrum of Activity of Commonly Used Second-Line


Antibiotic Dosa Streptococcus pneumoniae Haemoph Moraxe Anaero

ge Sensiti Intermedi Resist ilus lla bic
ve ate ant influenza catarrh bacteri
e alis a
Amoxicillin/clavu 500 +++ ++ + +++ +++ +++
lanate mg
Cefuroxime 250- +++ ++ + +++ ++ ++
Cefpodoxime 200 - +++ ++ + +++ +++
+ ++ - - +++ +++ -

cefixime mg/d
Ciprofloxacin 500- ++ + + ++ +++ +
Levofloxacin 500 +++ +++ +++ +++ +++ +++
Trovafloxacin 200 +++ +++ +++ +++ +++ +++
Clindamycin 300 +++ +++ +++ - - +++
Metronidazole 500 - - - - - +++
*+, low activity against microorganism; ++, moderate activity against microorganism; +++,
good activity against microorganism; -, no activity against microorganism

Patients with nosocomial acute sinusitis require adequate intravenous coverage of gram-
negative organisms. Aminoglycoside antibiotics are usually the drugs of choice for the
treatment of such patients because of their excellent gram-negative coverage and sinus
penetration. Selection of an antibiotic is usually based on the culture results of attained
maxillary secretion.

In addition to surgical management, complications of acute sinusitis should be managed with

a course of intravenous antibiotics. Third-generation cephalosporins (eg, cefotaxime,
ceftriaxone) in combination with vancomycin provide adequate intracranial penetration,
making them a good first-line choice.
Table 3. Dosage, Route, and Spectrum of Activity of Commonly Used Intravenous

Antibiotic Dosage Streptococc Haemophil Moraxell Gram- Anaerob

us us a negativ ic
pneumoniae influenzae catarrhal e bacteria
Piperacillin 3-4 g IV +++ + - +++ +++
Piperacillin/tazo 3.375 g IV +++ +++ +++ +++ ++
bactam q6h
Ticarcillin 3 g IV q4h +++ - - +++ ++
Ticarcillin/clavu 3.1 g IV +++ +++ - +++ ++
lanate q4h
Imipenem 500 mg IV +++ +++ +++ +++ +++
Meropenem 1 g IV q8h +++ +++ +++ +++ ++
Cefuroxime 1 g IV q8h +++ +++ +++ ++ ++
Ceftriaxone 2 g IV bid +++ +++ +++ +++ ++
Cefotaxime 2 g IV q4- +++ +++ +++ +++ ++
Ceftazidime 2 g IV q8h +++ +++ +++ +++ ++
Gentamicin 1.7 mg/kg - +++ +++ ++ -
IV q8h
Tobramycin 1.7 mg/kg - +++ +++ ++ -
IV q8h
Vancomycin 1 g IV q6- +++ - - - ++
*+, low activity against microorganism; ++, moderate activity against microorganism; +++,
good activity against microorganism; -, no activity against microorganism

Described below are recommended antibiotic regimens.

Class Summary

Therapy must be comprehensive and cover all likely pathogens in the context of this clinical

Amoxicillin (Trimox, Amoxil, Biomox)

First-line antibiotic. Interferes with synthesis of cell wall mucopeptides during active
multiplication, resulting in bactericidal activity against susceptible bacteria.

Cefdinir (Omnicef)

Classified as a third-generation cephalosporin and inhibits mucopeptide synthesis in the

bacterial cell wall. Typically bactericidal, depending on organism susceptibility, dose, and
serum or tissue concentrations.

Clarithromycin (Biaxin)

First-line antibiotic. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl

tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Cefuroxime (Ceftin, Kefurox, Zinacef)

Second-line PO and first-line IV antibiotic. Maintains gram-positive activity that first-

generation cephalosporins have; adds activity against P mirabilis, H influenzae, E coli, K
pneumoniae, and M catarrhalis.

Condition of patient, severity of infection, and susceptibility of microorganism determine

proper dose and route of administration.

Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy

against gram-positive organisms; higher efficacy against resistant organisms. Arrests
bacterial growth by binding to one or more penicillin binding proteins. Has good penetration.
Vancomycin (Vancocin, Lyphocin, Vancoled)

Potent antibiotic directed against gram-positive organisms and active against Enterococcus
species. Useful in the treatment of septicemia and skin structure infections. Indicated for
patients who cannot receive or have failed to respond to penicillins and cephalosporins or
who have infections with resistant staphylococci. For abdominal penetrating injuries, it is
combined with an agent active against enteric flora and/or anaerobes.

To avoid toxicity, current recommendation is to assay vancomycin trough levels after third
dose drawn 0.5 h prior to next dosing. Use CrCl to adjust dose in patients diagnosed with
renal impairment.

Used in conjunction with gentamicin for prophylaxis in penicillin-allergic patients

undergoing gastrointestinal or genitourinary procedures. Effective for resistant S pneumoniae.

Amoxicillin/Clavulanate (Augmentin)

Drug combination treats bacteria resistant to beta-lactam antibiotics.



Local complications

Mucoceles are chronic epithelial cysts that develop in sinuses in the presence of either an
obstructed sinus ostium or minor salivary gland duct. They have the potential for progressive
concentric expansion that can lead to bony erosion and extension beyond the sinus.

Maxillary sinus mucoceles are usually found incidentally on sinus radiographs and are of
little significance in the absence of symptomatology or infection. Surgical treatment is not
usually necessary, and these lesions often regress spontaneously over time.

Frontoethmoidal and sphenoethmoidal mucoceles, on the other hand, tend to be symptomatic

and have a high potential for bony erosion. Frontoethmoidal mucoceles should be completely
removed and the sinus obliterated. Sphenoethmoid mucoceles should be widely opened into
the nasal cavity.

Osteomyelitis is a potential local complication most commonly occurring with frontal

sinusitis. Osteomyelitis of the frontal bone is called a Pott puffy tumor and represents a
subperiosteal abscess with local edema anterior to the frontal sinus. This can advance to form
a fistula to the upper lid with sequestration of necrotic bone. This rare complication should be
managed with a combination of systemic antibiotics, surgical drainage of affected sinuses,
and debridement of necrotic bone.

Orbital complications

Orbital complications are the most common complications encountered with acute bacterial
sinusitis. Infection can spread directly through the thin bone separating the ethmoid or frontal
sinuses from the orbit or by thrombophlebitis of the ethmoid veins. Diagnosis should be
based on an accurate physical examination including ophthalmological evaluation and
appropriate radiological studies. CT scanning is the most sensitive means of diagnosing an
orbital abscess, although ultrasound has been found to be 90% effective for diagnosing
anterior abscesses.[10] The classification by Chandler, which is based on physical examination
findings, provides a reasonable framework to guide management. This classification consists
of 5 groups of orbital inflammation[11] :

Group 1 - Inflammatory edema (preseptal cellulitis) with normal visual acuity and
extraocular movement

Group 2 - Orbital cellulitis with diffuse orbital edema but no discrete abscess

Group 3 - Subperiosteal abscess beneath the periosteum of the lamina papyracea

resulting in downward and lateral globe displacement

Group 4 - Orbital abscess with chemosis, ophthalmoplegia, and decreased visual


Group 5 - Cavernous sinus thrombosis with rapidly progressive bilateral chemosis,

ophthalmoplegia, retinal engorgement, and loss of visual acuity; possible meningeal
signs and high fever

Medical management, including sinus drainage and intravenous antibiotics, is advocated for
any degree of orbital complication. The use of decongestant and antibiotic therapy is
discussed in the Medical Care and Medication sections.

Among the classifications by Chandler, surgical drainage of both the infected sinuses and the
orbit are advocated for groups 3-5 if inadequate improvement or progression of orbital
cellulitis occurs despite medical therapy or if the patient has loss of visual acuity. Surgical
procedures are discussed in Surgical Care.

Intracranial complications

Intracranial complications may occur as a result of direct extension through the posterior
frontal sinus wall or through retrograde thrombophlebitis of the ophthalmic veins. Subdural
abscess is the most common intracranial complication, although cerebral abscesses and
infarction that result in seizures, focal neurological deficits, and coma may occur. Intracranial
complications of sinusitis should be managed surgically with drainage of both the affected
sinus and the cranial abscess.

Subdural empyema is a life-threatening infection that may complicate acute sinusitis. Boto et
al (2011) reported the case of a previously healthy 10-year-old girl who developed subdural
empyema due to Gemella morbillorum infection after an untreated maxillary, ethmoidal, and
sphenoidal sinusitis.[12] Despite immediate drainage of the empyema and treatment with
broad-spectrum antibiotics, she developed frontal cerebritis and refractory intracranial
hypertension, needing urgent decompressive craniectomy. She recovered gradually with
slight right-sided hemiparesis and aphasia.

Systemic complications

Sinusitis can result in sepsis and multisystem organ failure caused by seeding of the blood
and various organ systems. Reports of bacteremia, thoracic empyema, and nosocomial
pneumonia have been documented in the intensive-care population with acute sinusitis, and
the mortality rate in this group can be as high as 11%. Fukushima et al (2012) reported on a
case of a 39-year-old man admitted for the onset of acute purulent meningitis.[13] A
cerebrospinal fluid culture grew Streptococcus sanguis. Sinusitis was found to be the cause of
the meningitis. Treatment with intravenous antibiotics was successful.


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14. [Guideline] Slavin RG, Spector SL, Bernstein IL, Kaliner MA, Kennedy DW, Virant
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18. Eibling DE. Maxillary Sinus: Irrigation Techniques. Myers EN, ed. Operative
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Nasal and Sublabial Approaches to the Pituitary


The transnasal-sublabial approach to the pituitary has undergone an evolutionary

refinement and today remains probably the most commonly used approach to selected
pituitary tumors. The following article describes the history, technique, and complications of
this useful surgical approach.

History of the Procedure

The evolution of the transnasal-transseptal approach to the pituitary traces its lineage and
subsequent reintroduction to sequential developments in rhinosurgical and neurosurgical

In 1909, Hirsch combined the septal-submucous resection (as reported by Killian and
Hajek's sphenoid sinusectomy) into a submucosal-septal approach to the sphenoid.[1] Halstead
first described using a gingivolabial incision to approach the septum, incorporating the upper
lip and nose as a composite flap.[2] In 1914, Cushing combined the gingivolabial incision and
submucous resection as an approach to the pituitary.[3] However, Cushing eventually
abandoned the transseptal procedure, citing the high risk of intracranial contamination that
likely results from direct contamination by the nasal vault.

In Paris, Guiot reported success using the transseptal approach, following the influence of
Cushing's pupil, Dott.[4, 5] Hardy subsequently reintroduced the transseptal procedure to North
America.[6] Combined with the advent of antibiotics, the use of intravenous steroids, and the
technological advancements in the use of the operating microscope, the transseptal approach
to the pituitary remains the most popular approach today.

The normal median sagittal nasal anatomy is shown in the image below.
Normal median sagittal nasal anatomy.


Pituitary adenoma (as seen in the image below)

Coronal and median sagittal images of pituitary adenoma.

Relevant Anatomy

Embryology, development, and surrounding anatomy of the sphenoid sinus

The sphenoid sinus begins as an evagination of the sphenoethmoidal recess during the
fourth month of fetal life. Following the third year of life, the sinus begins to excavate into
the pneumatizing sphenoid bone. This process progresses in the child from age 5-7 years. The
adult size is not reached until age 18 years.

The extent of pneumatization by the sinus into the sphenoid bone varies greatly. The
capacity of the sinus varies from 0.5-30 mL. Hamberger in 1961[7] and Congdon in 1930[8]
classified 3 differing types of sella pneumatization, and each is conceptualized by the position
in relation to the sella turcica. The presellar type (23%) has its posterior wall in contact with
the anterior face of the sella. The sellar or postsellar type (67%) appears when the sinus
extends posteriorly beyond the sella to the pons. The conchal type (5%) is similar to the
presellar type, except that the most posterior part of the sinus is well anterior to the sella

The paired sphenoid sinuses rarely are symmetrical in size and have an intersinus septum
that may be near horizontal in its orientation. This position renders the 2 sinuses in an over
and under orientation, rather than in a lateral orientation. Important central nervous system,
neurologic, and vascular structures surround the sphenoid sinus. Superiorly, the middle
cranial fossa and the pituitary gland are in approximation to the sinus, while anterosuperiorly,
the optic nerve and chiasm lie over the sinus. Anteriorly, a lateral margin of the sphenoid
bone forms a portion of the posterior orbital wall, and the anterior sphenoid forms a crest that
articulates with the perpendicular plate of the ethmoid bone.

The sphenoid ostia are located above the superior turbinate at approximately one-half the
length from the anteroinferior-most border of the sinus. The ostia drain into the posterior
aspect of the sphenoethmoidal recess. Laterally, the carotid artery may indent the sinus wall
posteroinferiorly or even lie within the sinus, directly contacting the sinus mucosa. Likewise,
the contents of the cavernous sinus, including the oculomotor, trochlear, and abducens nerves
and the ophthalmic and maxillary branches of the trigeminal nerve, contact the lateral wall of
the sinus. Inferiorly, the roof of the nasopharynx and the neurovascular anatomy of the
pterygoid canal are found. The inferior surface forms the sphenoid rostrum and articulates
with the vomer bone. Posteriorly, through the thick bony wall, the pons and basilar artery are


Contraindications to the transseptal-sublabial approach to the pituitary include the

Ongoing sinusitis that is untreated by either surgery and/or medical therapy

Highly vascular lesions

Dural-based lesions with a high risk for intraoperative and postoperative cerebrospinal
fluid leak

Lesions with extensive suprasellar extension and carotid artery anatomy, wherein the
arteries project into the sphenoid sinus and limit safe access


Imaging Studies

See the list below:

The preoperative workup for patients undergoing transphenoidal resection of the

pituitary includes a thorough history of sinus disease (eg, hyposmia, epistaxis, nasal
polyps, nasal discharge, sinusitis) and past nasal and sinus surgical treatment. Active
or untreated chronic sphenoid sinusitis is a contraindication to performing the
transphenoidal approach to the pituitary.

A CT scan is indispensable prior to performing any sinus surgery, and the transnasal-
sublabial approach to the sphenoid sinus is no exception. Perform preoperative
noncontrast-enhanced CT scanning in both the axial and the coronal planes. These
positions allow the surgeon to visualize essential sinus anatomic relationships. The
relationship of the perpendicular plate of the ethmoid bone to the sphenoid rostrum
and the presence and location of any intersinus septae are important anatomic
considerations. The CT scan also gives indication of any nasal or intrasinus pathology
that may require surgical or medical treatment prior to transphenoidal
hypophysectomy. Critical anatomic variations in the carotid artery or optic nerve can
also be observed from the CT scan.

MRI can help differentiate infectious etiology from mucocele formation in the sinus.
MRI studies may also help differentiate a possible vascular mass from the projection
of 1 or both carotid arteries into the sinus.

Coronal and median sagittal images are shown in the image below.
Coronal and median sagittal images of pituitary adenoma.

Treatment & Management

Surgical Therapy

The external rhinoplasty, transnasal transseptal, and transnasal sublabial approaches are
described below. The external rhinoplasty and transnasal approaches do not incorporate a
sublabial incision; however, the transnasal sublabial approach does.[9, 10]

External rhinoplasty approach

The external, or open, rhinoplasty approach for cosmetic or reconstructive rhinoplasty has
been used effectively in transsphenoidal hypophysectomy. Proponents of the external
approach described its unique ability to provide direct exposure to the sphenoid rostrum
because, unlike the sublabial approach, the overhanging lip obstruction is not present.
Moreover, because no oral incision is used, the external approach doesn't alter the
gingivobuccal sulcus, which can impede the use of dentures. In addition, without
superiorward elevation of the lip, upper lip paresthesia does not develop.[11, 12]

Furthermore, because no lateral dissection is necessary over the pyriform aperture or

resection of the maxillary spine or crest, incisor teeth paresthesia is less likely. Other
potential advantages include avoiding contamination from the oral cavity and avoiding
bleeding from the sublabial sulcus. Complications unique to the external approach include the
prolonged induration and edema of the nasal tip and an almost imperceptible columellar scar.
The open rhinoplasty approach incorporates the same surgical maneuvers as a cosmetic or
reconstructive procedure. Prior to injection with a local anesthetic that contains a
vasoconstrictor agent, the columellar incision is marked in an inverted gull-wing
configuration. Anesthetic agent is also injected into the vestibular skin just superior to the
most caudal margin of the lower lateral cartilage, the vestibular skin adjacent to the
intermediate crus and site of the columellar incision, and the interdomal area.

The septum is also injected in a submucoperichondrial plane on both sides to include the
vomer and perpendicular plate of the ethmoid bone. After 10 minutes, a #11 scalpel blade is
used to incise the columellar skin in the previously marked site. When making this incision,
note that the skin overlying the anterior face of the columella is extremely thin and care must
be taken not to incise the most caudal margin of the lower lateral cartilage medial crus.
Separate incisions are then made on the vestibular skin along the length of the lower lateral
cartilage that connects the columellar incisions to the domal region.

Dissection is then carried superiorly in a plane immediately superficial to the lower lateral
cartilage until the domal region, and only laterally over the most caudal margin of the lower
lateral cartilage as necessary to gain access to the nasal tip. The interdomal ligaments are
divided and the anterior septal angle and caudal end of the quadrangular cartilage are then
visualized. The mucoperichondrial flaps are then elevated on either side of the quadrangular
cartilage from the caudal margin of the cartilage to the perpendicular plate of the ethmoid
bone and vomer. If the neurosurgeon needs cartilage, it is harvested while a 1-cm continuous
cartilaginous dorsal and columellar strut is maintained. Further cartilage, vomer, and the
perpendicular plate of the ethmoid bone is resected to visualize the sphenoid rostrum, and any
remaining cartilage on the maxillary crest is removed to allow neurosurgical speculum

Because the open rhinoplasty approach necessarily relies on the disruption of normal
structural nasal support mechanisms, these must be reconstituted at the end of the procedure.
Chief among these anatomic supports that require reconstitution include the interdomal
ligaments and the support provided by the columella. At minimum, a 5-0 polydioxanone
(PDS) suture should be used to reconstruct the interdomal ligaments with a portion of
cartilage from the quadrangular cartilage used as a columellar strut. Final closure of the
columellar incision is initiated using a single deep 5-0 PDS suture followed by interrupted 7-
0 nylon skin sutures. All endonasal incisions are then closed with interrupted 4-0 chromic
suture. Silastic septal splints are then applied to each of the mucoperichondrial planes with a
running 4-0 nylon suture.

Transnasal transseptal approach

Unlike the external rhinoplasty approach, the transnasal transseptal approach requires no
external columellar incision. Instead, a hemitransfixion incision is made, and the right and
left mucoperichondrial flaps are then elevated over the quadrangular cartilage and
perpendicular plate of the ethmoid and vomer bones. The mucoperichondrial flaps are
elevated continuously with the mucoperiosteal flaps onto the floor of the nose. While
maintaining a 1-cmwide continuous dorsal and caudal cartilaginous strut, a portion of the
quadrangular cartilage is resected and subsequently used to close the sphenoid defect. The
caudal cartilaginous strut is then disarticulated from the maxillary crest and displaced
laterally. Further ethmoid and vomer bone is resected with any remaining cartilage on the
maxillary crest to allow sphenoid rostrum visualization. If exposure is limited because of a
small nasal aperture, a unilateral alotomy can be made ipsilateral to the side of speculum

Transnasal-sublabial approach to the sphenoid sinus

The operation may be conceptualized as having nasal, septal, and oral portions, with the
nasal surgical procedure performed before the oral portion. For the nasal septal portion of the
operation, 2 separate approaches are described. One approach elevates the
mucoperichondrium from both right and left faces of the septum, vomer, and perpendicular
plate of the ethmoid bone, with subsequent harvest of a defined piece of quadrangular
cartilage. The other approach leaves mucoperichondrium attached to one side of the cartilage
to create a composite mucoperiosteal-quadrangular flap that is displaced laterally.

The patient is placed supine on the operating room table, and a Mayfield headrest is
applied. The neurosurgeon should assist the otolaryngologist in defining the head position to
avoid further unnecessary manipulation of the patient's cranium. Subsequently, neurosurgical
pledgets containing 4% cocaine are placed into each nasal vault, with 1 in the
sphenoethmoidal recess and the others overlying the middle and inferior turbinates. Local
anesthetic consisting of 1% lidocaine containing 1:100,000 epinephrine is injected bilaterally
into the nasal-septal submucoperichondrial plane, the subperiosteal plane of the vomer, and
the perpendicular plate of the ethmoid bone. The lidocaine is also injected bilaterally into the
floor of the nose and into the gingivolabial sulcus anteriorly between the canine teeth.

The eyes are covered with a transparent occlusive dressing that allows visualization of the
periorbita and palpation of the globe during the procedure. The head and face are draped, and
the eyes, nose, and mouth remain exposed. The cocaine pledgets are removed, and the first
incision is made.

Preoperative Details

The surgeon performing the operation, not the neurosurgeon, should explain the risks and
complications of the transnasal-sublabial approach in detail. The most common risks and
complications of the procedure include the following:

Marked edema and cosmetic deformity of the midface, which may last up to 6 months
or be permanent in nature

Decreased sensation over the entire mid face and/or teeth, which may last up to 6
months or be permanent in nature

Cosmetic deformity of the external nasal skeleton, which may require further
cosmetic and reconstructive surgery

Difficulty breathing through the nose, which may require further reconstructive
surgery and may be permanent in nature

Nasal-septal perforation, which may require further reconstructive surgery and may
be permanent in nature

Chronic nasal dryness and/or bleeding

Complete or partial loss of the sense of smell

Cerebrospinal fluid leak, which may require further surgery to correct

Double vision or complete blindness, which may be temporary or permanent in nature

Complete or partial loss of skin over the mid face, which may require further
reconstructive surgery
Complete or partial breakdown of the gingivolabial incision requiring additional oral
surgical procedures

Injury to the gingiva requiring extensive oral surgical reconstructive surgery

Difficulty wearing oral appliances (eg, dentures) after healing is complete, which may
necessitate revision of the appliances or reconfiguration of new appliances

Intraoperative Details

Nasal-septal procedure

The median, sagittal, and coronal anatomy is represented in the images below and is the
orientation for the following discussion.

Normal median sagittal nasal anatomy.

Normal coronal nasal anatomy.

Approach with cartilage removal

The neurosurgeon often requires a portion of quadrangular cartilage to reconstruct the

sphenoid. The procedure is initiated with a hemitransfixion incision made into either the right
or left mucoperichondrial plane and carried down to the level of the septal cartilage as seen in
the image below. This submucoperichondrial plane develops and is elevated from the
quadrangular cartilage to its junction with the vomer and the perpendicular plate of the
ethmoid bone. Inferiorly, this plane attaches to the maxillary crest and elevates from the nasal
floor. Through the same incision caudally, the contralateral mucoperichondrial plane is
elevated from underlying structures as mentioned above.
Elevation of septal mucoperichondrial-periosteal flap.

Coronal view of septal mucoperichondrial flap elevation.

An incision is then made into the cartilage in a continuous L-shaped configuration, while
maintaining a 1-cm width in both caudal and dorsal dimensions. The cartilage is removed
using a swivel knife and cleanly excised from its junction at the perpendicular ethmoid bone,
vomer, and maxillary crest and spine. Thus, a significant portion of quadrangular cartilage
may be harvested as long as the remaining portion is one continuous piece that is 1 cm in
dorsal and caudal width and remains attached to the keystone area (attachment of
quadrangular cartilage to nasal bone pyramid) under the caudal edge of the nasal bone.

If the remaining strut of cartilage is detached from this critical site, the cartilage must be
sutured back into position. Failure to permanently maintain this support is likely to result in a
saddle-nose deformity. Finally, if the neurosurgeon does not use this portion of harvested
cartilage in its entirety to reconstruct the sphenoid, then the cartilage may be replaced
between the mucoperichondrial layers prior to closure.

Following removal of a portion of cartilage, the fibrous adhesion between the septal
mucoperichondrial plane and the maxillary crest may be carefully incised with the sharp end
of a Cottle or Freer elevator. A submucoperiosteal plane is then developed onto the floor of
the nose. The same technique is performed on both sides, such that one continuous flap is
developed on each side that begins superiorly near the dorsum and ends subperiosteally on
the floor of the nose as seen in the image below. Alternatively, the nasal floor
submucoperiosteal plane may be developed after making the gingivolabial incision. In this
case, carefully dividing the fibrous attachments between the nasal floor submucoperiosteal
flap and the septal mucoperichondrial flaps at the maxillary crest may serve to connect these

Continuous septal mucoperiosteal and nasal floor mucoperiosteal flaps.

Approach without cartilage removal

If cartilage harvest is not anticipated, then elevation of the mucoperichondrial plane is

initiated on only one side of the cartilaginous septum. Elevation is carried out over the
ipsilateral face of the vomer, the perpendicular ethmoid bone, and inferiorly to the maxillary
crest. The dissection is carefully carried through the fibrous attachments at the maxillary crest
and onto the ipsilateral floor of the nose as seen in the image below, elevating a
submucoperiosteal plane. Thus, a flap is created on one side that includes in continuity both
the septal mucoperichondrial and nasal floor mucoperiosteal flaps.

Through the preexisting hemitransfixion incision, an inferior tunnel is created in the nasal
floor on the contralateral side. This tunnel extends laterally from under the inferior turbinate
to the maxillary crest medially. The tunnel extends anteriorly from the nasal aperture to
nearly the posterior end of the hard palate. This is represented in the image below.
Continuous septal and nasal flaps and contralateral nasal floor flap.

A vertical incision is made into the quadrangular cartilage, making certain that a
significant portion of cartilage remains attached to the perpendicular plate of the ethmoid
bone and the underside of the nasal bones in the keystone region. Failure to maintain these
attachments allows the inferior displacement of the cartilaginous dorsum, which results in a
saddle-nose deformity. A long-blade nasal speculum is inserted between the continuous
mucoperichondrial and mucoperiosteal flaps, and the fibrous attachments between the
maxillary crest and septal cartilage are divided. Use particular care when the cartilage is
dissociated from the maxillary crest and when connecting the composite flap with the
contralateral nasal floor mucoperiosteal flap. The cartilage is dissociated from its bony
attachments at the vomer. The perpendicular plate of the ethmoid bone, the maxillary crest,
and the composite flap are then mobilized laterally into the same nasal vault. This is
represented in the image below.
Transection of septal cartilage, vomer, and ethmoid bones.

The speculum is placed into the posterior cartilaginous incision. After inferior and
superior vomer and perpendicular plate bony cuts are made with septal scissors, the
perpendicular plate of the ethmoid bone and vomer are removed with a Takahashi or Jansen-
Middleton forceps. The bone is removed until the sphenoid rostrum is exposed.

Modified approach for narrow space

Takemura et al described a modified transnasal transseptal approach to pituitary lesions, a

two-surgeon, four-handed technique for use in patients with a narrow nasal space. In this
procedure, a transseptal route was taken through one nostril, with an endoscopic septoplasty
technique employed to remove the nasal septum; a transnasal approach was used via the other
nostril, with no pedicled nasoseptal flap harvested on that side. However, the surgeons
preserved the transnasal-side mucosa containing the septal branch of the sphenopalatine
artery located over the face of the sphenoid and nasal septum; in this way, a nasoseptal flap
could be harvested if an intraoperative cerebrospinal fluid leak occurred. The modified
procedure was carried out on six patients, each of who had a pituitary lesion (nonfunctioning
macroadenoma, Rathke cleft cyst, or growth hormone-producing macroadenoma), as well as
a severely deviated nasal septum and/or narrow nasal space. The operations were performed
without surgicalcomplications.[13]
Oral surgical procedure

The nasal speculum is removed, and attention is directed to the gingivolabial sulcus. An
incision is made in the sulcus approximately 1 cm superior to the gingival margin between
canine fossae. Gingivolabial incision is depicted in the image below.

Gingivolabial incision.

Double pronged hooks or a wide rake are then placed in this gingivolabial incision, and
dissection is carried superiorly in a subperiosteal plane to the pyriform aperture. Next, careful
dissection occurs at the inferior most margin of the pyriform aperture, and the
mucoperiosteum is elevated bilaterally off the floor of the nose. The mucoperiosteum sweeps
laterally under the inferior turbinates and posteriorly to the midnasal floor. Any attachments
of the caudal septum with the maxillary spine are divided in the process.

Exposure of sphenoid rostrum

o A neurosurgical speculum is inserted through the sublabial incision, as seen in

the image below, between the septal mucoperichondrial mucosal flaps (or in
between the septal mucoperichondrial and composite septal flaps in the
instance where cartilage is not harvested).
Insertion of speculum through gingivolabial incision.

o The speculum is advanced superiorly to the level of the well-exposed sphenoid

rostrum. Wide exposure of the rostrum is best achieved with a neurosurgical
speculum that has flanged blade tips because these tips push the previously
elevated sphenoid rostrum mucoperiosteum laterally. The blades of the
speculum are then opened widely, and intraoperative fluoroscopic radiography
confirms the correct position of the speculum. The remaining portions of
vomer and ethmoid bone are removed, which allows the speculum to contact
the sphenoid rostrum as seen in the image below.

Placement of speculum after

removal of septal cartilage and bone.
o With the radiographic confirmation of the proper speculum position, an
osteotome and Gay-Kerrison rongeur are used to enter the sphenoid sinus in
the midsagittal plane. Careful removal of the rostrum is performed to achieve
a full view of the sphenoid sinus. With the sphenoid sinus opened, the
remainder of the operation is turned over to the neurosurgeon.

Approach after previous nasal-septal surgery

Patients who have planned sublabial-transphenoidal surgery often have had previous nasal-
septal, maxillary, or sinus surgical procedures. The concern is that clean dissection between
tissue planes may be difficult or impossible because the surgeon encounters a large amount of
scar tissue. This concern especially is relevant when the patient has had previous septal
surgery (eg, submucous cartilage resection, or septoplasty). Careful dissection between
mucoperichondrial planes can be difficult, if not impossible. A number of possible
alternatives exist for the patient that has had previous septal surgery. Conceptually, the
surgeon may carefully dissect through or around the cicatrix or laterally displace the septum
to expose the sphenoid rostrum. Each approach is considered individually below.

Dissection through previous cicatrix: Following a carefully executed hemitransfixion

incision, difficult dissection through adherent mucoperichondrial planes can be
facilitated with a narrow-width long-bladed nasal speculum. After establishing a
dissection plane anteriorly between mucoperichondrial planes, this speculum is
carefully insinuated. Both blunt and sharp dissection take place under well-lit direct
visualization to meticulously dissect the planes. This is one dissection that relies on
absolute visualization and not on the feel between planes. Often, if the dissection
becomes nearly impossible because of densely adherent tissue planes, redirecting the
dissection to a more superior or inferior plane reveals a place to reestablish the

Dissection around the cicatrix: Using a hemitransfixion incision, unyielding adherent

mucoperichondrium may be dissected free over or under the cicatrix to arrive at the
sphenoid rostrum. The adherent mucoperichondrium often exists in multiple regions,
which contributes to inadequate neurosurgical exposure. The open or external
rhinoplasty approach is advocated when multiple sites of cicatrix limit the safe and
adequate dissection between mucoperichondrial planes.
Lateral dislocation of the septum:

o Lateral dislocation of the septum is a third alternative when other techniques

cannot be used because the mucoperichondrial planes are sufficiently adherent
or when the risk that a significant septal perforation may occur following
attempted dissection is too great. In this technique, an incision is made along
the nasal floor, as seen in the image below, just under the inferior turbinate.
The incision extends from the pyriform aperture to the junction of the hard and
soft palate.

Incision through nasal floor.

o The mucoperiosteum is elevated to the maxillary crest, and the attachments

between the septum and maxillary crest are divided. This incision is then
connected anteriorly to almost the entire circumference of a full transfixion
incision. This is represented in the image below.
Medialization of nasal floor flap.

o As the septal flap is dislocated laterally into the contralateral nasal vault, a
vertical incision is made through the mucosa overlying the vomer bone, and
the midline is identified inferior to the floor of the sphenoid bone. Through
this opening, the sphenoid rostrum is identified. After the sublabial flap is
elevated, the septal flap is dislocated laterally, the neurosurgical speculum is
inserted up to the level of the sphenoid rostrum, and entrance is made into the
sphenoid sinus.

Closure of nasal-septal and oral incisions

The nasal portion of the closure precedes the oral closure. Fixing the anterior-inferior septal
cartilaginous strut to the maxillary spine with 4-0 PDS suture initiates nasal closure. Often,
the maxillary spine and large portions of the maxillary crest have been resected to obtain
superior visualization of the sphenoid rostrum, leaving little bony or durable soft tissue with
which to affix suture. In these cases, the septal cartilage may be sutured instead to the soft
tissues of the columella. Cartilage strips may also be used as a columellar strut to add support
and prevent postoperative nasal tip ptosis.
The hemitransfixion incision is closed with a continuous running 4-0 chromic suture, and the
mucoperichondrial flaps are reapproximated with silastic splints. The splints are placed one
on each side and are quilted together using a 4-0 nylon suture. The nasal vault is packed on
each side with a nonabsorbable sponge coated with antibiotic ointment. The sponge is
removed on the fourth postoperative day. The gingivolabial incision is then closed using both
deep and mucosal interrupted 3-0 chromic sutures.

Postoperative Details

Nasal packing and septal splints are removed in the first week postoperatively. Patients are
reminded to use an intranasal saline mist 4-6 times per day for 2-3 weeks postoperatively to
minimize intranasal crusting.

The otolaryngologist-head and neck surgeon evaluates the patient postoperatively at weekly
intervals for a total of 4 visits. This schedule allows for thorough clearing of nasal crusting
and obstruction under direct visualization.


The oral and rhinologic sequelae and complications arising from the sublabial-transseptal
approach to the sphenoid essentially are the same as those for any gingival and septal surgery.
These complications can be conceptualized separately as those arising from the nasal and
those arising from the oral surgical portions of the procedure.

Nasal complications

Perhaps the most common complication is septal perforation.[14] In 1990, Gammert conducted
a 5-year follow-up study of patients undergoing either intranasal-transseptal or sublabial-
transseptal approach and found a 12.4% perforation rate.[15] This rate is significantly higher
than the 5-8% reported in the rhinologic literature. Rhinologic studies report that patients
with prolactinoma have a higher incidence of septal perforation than those with acromegaly.
This difference is attributed to a difference in mucosal atrophy, a phenomenon observed in
patients with pituitary gland dysfunction.

Mucosal dryness or nasal crusting was noted in 35.4% (n=113) of patients undergoing
transnasal or translabial approaches. These patients required moistening ointments and nasal
spray as therapy. Frank epistaxis is an infrequent complication of any approach to the
sphenoid and, in one series, was observed in 3.5% of patients.
Oral surgical complications

Detractors of the sublabial approach mention the complication of upper lip, dental, and
gingival hypesthesia. This hypesthesia presumably is the result of division of cranial nerve X
as it courses through the incisive foramen and supplies the upper lip and central incisors.
Injury to this nerve is likely to occur when the nasal spine is reduced in size or removed
completely to better visualize the sphenoid rostrum. While some authors believe this
complication is more likely to occur with the sublabial approach, it also is a likely
complication of any transphenoidal approach when removal of the nasal spine is performed to
better visualize the sphenoid rostrum. Return of partial or complete sensation is likely to
occur by the sixth month postoperatively if it returns at all.

Division of the gingivolabial mucosa with subsequent cicatrix can impair proper fitting of
dentures by fibrotic tissue obliteration. Explain to patients that, even after postoperative
tenderness has resolved fully, dentures might require either adjustment or complete
replacement to account for this change in anatomic contour.

1. Hirsch O. Eine neue methode der endonasalen operation von ypophysentumoren.

Wien Med Wochenschr. 1909. 59:636-638.

2. Halstead AE. Remarks on the operative treatment of tumors of the hypophysis: with a
report of two cases operated on by an oro-nasal method. Surg Gynecol Obstet. 1910.

3. Cushing H. Surgical experiences with pituitary disorders. JAMA. 1914. 63:1515-1525.

4. Guiot G. Indications for the trans-sphenoidal approach of the hypophyseal fossa.

Rhinol. 1973. 11:137-152.

5. Dott N, Bailey A. A consideration of the hypophysial adenomata. Br J Surg. 1925.


6. Hardy J. Transsphenoidal hypophysectomy. J Neurosurg. 1971 Apr. 34(4):582-94.


7. Hamberger CA, Hammer G, Norlen G, Sjogren B. Transantrosphenoidal

hypophysectomy. Arch Otolaryngol. 1961 Jul. 74:2-8. [Medline].

8. Congdon ED. The distribution and mode of origin of septa and walls of the sphenoid
sinus. Anat Rec. 1930. 18:97.

9. Lazaridis N, Natsis K, Koebke J, Themelis C. Nasal, sellar, and sphenoid sinus

measurements in relation to pituitary surgery. Clin Anat. 2010 Sep. 23(6):629-36.

10. Chole RA, Lim C, Dunham B, Chicoine MR, Dacey RG Jr. A novel transnasal
transsphenoidal speculum: a design for both microscopic and endoscopic
transsphenoidal pituitary surgery. J Neurosurg. 2011 May. 114(5):1380-5. [Medline].

11. Duz B, Harman F, Secer HI, Bolu E, Gonul E. Transsphenoidal approaches to the
pituitary: a progression in experience in a single centre. Acta Neurochir (Wien). 2008
Nov. 150(11):1133-8; discussion 1138-9. [Medline].
12. Neal JG, Patel SJ, Kulbersh JS, Osguthorpe JD, Schlosser RJ. Comparison of
techniques for transsphenoidal pituitary surgery. Am J Rhinol. 2007 Mar-Apr.
21(2):203-6. [Medline].

13. Takemura M, Fujimoto Y, Kobayashi T, et al. A modified combined

transseptal/transnasal binostril approach for pituitary lesions in patients with a narrow
nasal space: technical note. Neurol Med Chir (Tokyo). 2014. 54(8):622-8. [Medline].

14. Er U, Grses L, Saka C, Belen D, Yigitkanli K, Simsek S, et al. Sublabial transseptal

approach to pituitary adenomas with special emphasis on rhinological complications.
Turk Neurosurg. 2008 Oct. 18(4):425-30. [Medline].

15. Gammert C. Rhinosurgical experience with the transseptal-transsphenoidal

hypophysectomy: technique and long-term results. Laryngoscope. 1990 Mar.
100(3):286-9. [Medline].

16. [Guideline] Cook DM, Ezzat S, Katznelson L, Kleinberg DL, Laws ER Jr, Nippoldt
TB, et al. AACE Medical Guidelines for Clinical Practice for the diagnosis and
treatment of acromegaly. Endocr Pract. 2004 May-Jun. 10(3):213-25. [Medline].

17. Cook DM, Ezzat S, Katznelson L, Kleinberg DL, Laws ER Jr, Nippoldt TB, et al.
AACE Medical Guidelines for Clinical Practice for the diagnosis and treatment of
acromegaly. Endocr Pract. 2004 May-Jun. 10(3):213-25. [Medline].

18. Cushing H. Partial hypophysectomy for acromegaly. Ann Surg. 1909. 50:1002.

19. Dew LA, Haller JR, Major S. Transnasal transsphenoidal hypophysectomy: choice of
approach for the otolaryngologist. Otolaryngol Head Neck Surg. 1999 Jun.
120(6):824-7. [Medline].

20. Hollinshead WH. Anatomy for Surgeons. 3rd ed. Philadelphia, Pa: Harper & Row.

21. Koltai PJ, Goufman DB, Parnes SM, Steiniger JR. Transsphenoidal hypophysectomy
through the external rhinoplasty approach. Otolaryngol Head Neck Surg. 1994 Sep.
111(3 Pt 1):197-200. [Medline].

22. Sawyer R. Nasal approach to the sphenoid sinus after prior septal surgery.
Laryngoscope. 1991 Jan. 101(1 Pt 1):89-91. [Medline].
23. Schoem SR, Khan A, Wilson WR, Laws ER. Minimizing upper lip and incisor teeth
paresthesias in approaches to transsphenoidal surgery. Otolaryngol Head Neck Surg.
1997 Jun. 116(6 Pt 1):656-61. [Medline].
Nasal Polyp Surgery


Polyp formation in the nasal cavity is due to chronic allergic rhinitis, chronic sinusitis, and,
less commonly, underlying disease such as cystic fibrosis. Patients usually present with nasal
obstruction, persistent nasal discharge (rhinorrhea), sinus infection, and loss of the sense of
smell (anosmia) of prolonged duration.

History of the Procedure

Knowledge of nasal polyposis extends to medical antiquity. The disease process was
mentioned in Egyptian and Indian medical treatises 2500-3000 years ago.

Through the ages, several treatments have been advocated, including cautery with hot irons,
application of caustic chemical substances, abrasion by drawing rags through the choanae and
out the nose, and snaring.

Today, the standard surgical therapy is endoscopically guided removal of diseased tissues
with preservation of maximal amount of normal nasal mucosa.


Patients usually have chronic nasal symptoms prior to detection of nasal polyps.



The frequency of nasal polyps is uncertain. Only 0.5% of individuals with atopic symptoms
manifest nasal polyposis, and most patients with diffuse nasal polyposis do not demonstrate
an immunoglobulin E (IgE)mediated type 1 hypersensitivity reaction. Patients with cystic
fibrosis have a higher prevalence of nasal polyposis (up to 40%).


Polyp development within nasal and sinus regions implicates an IgE-type hypersensitivity
and an immunologic or possibly inflammatory basis for such formation.
The exact etiology of polyp formation is unknown. Research is demonstrating an eosinophil-
mediated mechanism with damage to the mucosa by major basic protein, but the complicated
interplay of secondary messengers and chemical mediators is not clear.

Nasal polyposis in association with cystic fibrosis, sinobronchial syndrome, aspirin

sensitivity, and Samter triad (asthma, aspirin allergy, nasal polyposis) indicates manifestation
of nasal mucosal damage by many different possible disease processes.


The polyp surface consists of pseudostratified respiratory epithelium and is subject to

metaplasia due to local pressure and trauma. Polyps can undergo fibrosis and


Patients present with nasal airway obstruction, chronic rhinosinusitis, exacerbation of asthma,
and nasal and facial deformity (rarely).[2, 3]
Patients may also present with bleeding and
anosmia. Not insignificantly, these patients may have undergone recurrent surgery and costly
medical therapy.


The patient may require surgical intervention if severe symptoms of obstruction and infection
prove refractory to medical treatment.

Medical therapies include treatment for underlying chronic allergic rhinitis using
antihistamines and topical nasal steroid sprays. For severe nasal polyposis causing severe
nasal obstruction, treatment with short-term steroids may be beneficial. Topical use of
cromolyn spray has also been found to be helpful to some patients in reducing the severity
and size of the nasal polyps.

Within the nasal and sinus region, polyps originate from the middle meatus/ostiomeatal
complex. With surgical removal of diseased tissues (polyps), future recurrence of polyp
formation is still possible. In endoscopic sinus surgery, the goal is to remove diseased tissue
and provide adequate sinus aeration in order to prevent recurrence.

Relevant Anatomy
Nasal polyps can develop in all the paranasal sinuses, but the region of middle
meatus/osteomeatal complex lateral to the middle turbinate is of great importance.


Severe pulmonary or cardiac problems may be contraindications to surgical treatment.

Relative contraindications to surgical treatment include bleeding diathesis (which can be
medically treated before surgery), acute asthma exacerbation, and the patient's inability or
unwillingness to obtain appropriate postoperative follow-up care and treatment.


Laboratory Studies

See the list below:

Relevant allergy or asthma studies (if indicated)

Nasal smears or cultures for fungus and bacteria (if indicated)

Imaging Studies

See the list below:

CT scan of sinuses without contrast: Specify coronal CT with 3-4 mm cuts and
appropriate soft tissue and bone windows.

o Evaluate the CT scan results with attention to anterior ethmoid artery, orbital
and skull base anomalies, optic nerve and carotid in posterior ethmoidal
(Onodi) cells, and sphenoid sinus.

o Focus especially on previous surgical changes. Consider role and use of

image-guidance system in revision or difficult cases.[4]

Other Tests

See the list below:

Olfactory testing (if indicated)

Medical workup for cystic fibrosis (if indicated)

Diagnostic Procedures

See the list below:

A nasal and sinus endoscopy with evaluation of anatomy, site of origin, past surgical
changes, and evidence of other disease-causing polyps (tumor, infection, systemic
diseases such as Sarcoidosis, Wegener granulomatosis) may be appropriate (see Nasal
Polyps, Nonsurgical Treatment).

Histologic Findings

Pseudostratified epithelium is usually found. Pay special attention to unilateral polyps that
may be neoplastic, and examine them for malignancy or possible malignant transformation of
benign neoplasia(20% in inverting papilloma).


Staging is relevant in inverted papilloma with malignant transformation.

Treatment & Management

Medical Therapy

The following medical treatments are available (see Nasal Polyps, Nonsurgical Treatment):

Topical steroid inhaler

Topical antihistamine inhaler

Systemic steroids

Intranasal cromolyn treatment

Treatment and control of allergic rhinitis

Treatment of underlying sinusitis

Surgical Therapy

Endoscopic sinus surgery is the procedure of choice. With the advent of endoscopic sinus
surgery, surgical treatment for sinus diseases has become safer, and the outcome has
improved. Results following nasal polypectomy are no better than nasal polypectomy with
endoscopic sinus surgery and are worse for patients with Samter's triad.[5] With appropriate
preoperative evaluation and planning, endoscopic sinus surgery is usually carried out in an
ambulatory setting with minimal discomfort to patients.

Sinus surgery can be carried out under local anesthesia with sedation or general anesthesia.
Intraoperatively, extreme care must be exercised to avoid orbital and neurologic
complications. The preoperative CT scan serves a vital role in proper evaluation of potential
anatomic anomalies and changes due to disease process or anatomic variance.

Patients undergoing preoperative consultation must be informed of potential orbital

complications, the possibility of postsurgical cerebrospinal fluid leakage, possible bleeding
from related sinus arteries, and the possibility of polyp recurrence despite surgical removal.
Patients should also be counseled regarding the need for close follow-up care and
postoperative medical treatment for allergy, asthma, and other related medical conditions.

Preoperative Details

Careful review of the CT scan results preoperatively and the availability of CT scans during
the procedure are important for a successful outcome.

Inform the patient that the recovery of the sense of smell is unpredictable and is not
guaranteed, even with proper surgical and medical treatment. Stress the importance of
continual postoperative treatment of allergic rhinitis and chronic nasal conditions to ensure
long-term success and prevent polyp re-formation.

Intraoperative Details

Proper instrumentation and methodical sinus surgery lead to decreased complications and a
positive outcome of the surgical treatment. Surgical specimens are sent for pathological

Debridement may reduce intraoperative blood loss.[6] Nasal packing material is recommended
to minimize postoperative bleeding from the sinuses and nose.

Recent advent of a computerized CT tracking system to better define important surgical

anatomical sites during surgery in real time has been useful to avoid potential complications
in selected potential complex cases. Complex surgical cases include history of prior/repeat
sinus surgery, potential orbital and/or brain involvement of disease process, and other pre-
existing anatomical variants.

However, CT guidance surgery is not recommended for all sinus surgery cases. Medical
judgment and careful patient selection will enhance the benefit for new technology in sinus

Proper training and surgical techniques are paramount to ensure patient safety in all sinus
surgeries. New technology should always be adjunct to careful surgical planning and
implementation of treatment decision making.

Postoperative Details

Stress the importance of close follow-up care and debridement of the sinuses and nasal
cavity. Resume medical treatment and control of allergic rhinitis to prevent polyp recurrence.

It is not uncommon that patients may have good immediate postsurgery results in relief of
nasal obstruction; however, loss to medical follow-up and lack of medical treatment
postsurgery may mean not detecting the recurrence of polyposis.

Patient education regarding the long-term treatment plan and goal should be stressed. The
need for long term treatment to prevent the recurrence of polyposis should be conveyed to all


Guidelines for follow-up care are as follows:

Day 1-2 - Removal of nasal packing and debridement of sinuses and instruction for
patient's self-care at home with topical antibiotic ointment

Day 4-5 - Inspection and debridement of sinuses to ensure proper healing

Day 10 - Inspection and debridement of sinuses and resumption of medical treatment

with nasal steroid inhaler

2-3 weeks - Inspection and debridement of sinuses to ensure complete healing of

nasal and sinus mucosa

5-6 weeks - Inspection and routine follow-up and medical care

3 months - Inspection and routine follow-up and medical care

After the above protocol, follow-up care in 4- to 6-month intervals should be sufficient.

These guidelines may be individualized according to the clinical progress of the patient and
severity of disease prior to surgery.


Major complications include the following:

Central nervous system - Surgery-related cerebrospinal fluid leak, meningitis,

intracranial hemorrhage, brain abscess, brain herniation

Orbit - Blindness, optic nerve injury, orbital hematoma, eye muscle injury leading to
diplopia, nasolacrimal duct injury leading to epiphora

Vascular - Vascular injury leading to severe hemorrhage


Outcome and Prognosis

With proper patient selection for surgical treatment, sinus surgery offers a good outcome and
long-term relief for patients.

Proper preoperative counseling and education for patients regarding the importance of long-
term follow-up and medical treatment will minimize the chance of polyp recurrence.[7, 8]

A study by Nguyen et al found that endoscopic surgery for nasal polyposis improved
moderate to severe facial pain/headache in approximately 60% of patients reporting these
symptoms. The study included 107 patients with nasal polyposis, 52.33% of whom were
suffering moderate to severe facial pain/headache prior to surgery. Six weeks postoperatively,
20.56% of the 107 patients were still experiencing this level of pain, necessitating neurologic
counseling to determine whether it had a non-sinonasal cause.[9]

A prospective study by Brescia et al indicated that in patients who undergo endoscopic

surgery for chronic rhinosinusitis with nasal polyps (CRSwNP), the polyps are more likely to
recur in cases of eosinophilic-type CRSwNP. The study, which included 143 patients, also
found that nasal polyps recurred more quickly in eosinophilic-type CRSwNP than in the non-
eosinophilic type.[10]

Future and Controversies

Improvement is needed in the treatment of chronic allergic rhinitis and associated nasal
conditions. Good initial results have been noted with medical treatment combined with nasal
steroid plus nasal cromolyn treatment to decrease the size and formation of nasal polyps.

Chemical mediators, antifungal substances, leukotriene, and interleukin inhibitors are being
investigated and may have a role in future treatment for nasal polyposis.

Continual advances in medical and surgical technology with support from a computerized
guidance imaging system during sinus surgery will continue to improve the outcome and
safety of surgical sinus treatment.

However, technological advancement should never replace good and sound judgment for
surgical treatment recommendation by experienced and qualified ENT specialists.

1. Tang J, Liu S, Zhang L, Chen W, Shi S, Yu Q, et al. Correlation analysis of

prognostic and pathological features of patients with chronic sinusitis and nasal
polyps following endoscopic surgery. Exp Ther Med. 2013 Jul. 6(1):167-171.
[Medline]. [Full Text].

2. Deal RT, Kountakis SE. Significance of nasal polyps in chronic rhinosinusitis:

symptoms and surgical outcomes. Laryngoscope. 2004 Nov. 114(11):1932-5.

3. Fokkens W, Lund V, Mullol J. European position paper on rhinosinusitis and nasal

polyps 2007. Rhinol Suppl. 2007. (20):1-136. [Medline].

4. Kingdom TT, Orlandi RR. Image-guided surgery of the sinuses: current technology
and applications. Otolaryngol Clin North Am. 2004 Apr. 37(2):381-400. [Medline].

5. Mendelsohn D, Jeremic G, Wright E, Rotenberg E. Revision Rates After Endoscopic

Sinus Surgery: A Recurrence Analysis. Ann Otol Rhinol Laryngol. March 2011.

6. Kumar N, Sindwani R. Bipolar microdebrider may reduce intraoperative blood loss

and operating time during nasal polyp surgery. Ear Nose Throat J. 2012 Aug.
91(8):336-44. [Medline].

7. Bassiouni A, Wormald PJ. Role of frontal sinus surgery in nasal polyp recurrence.
Laryngoscope. 2013 Jan. 123(1):36-41. [Medline].

8. Vento SI, Blomgren K, Hytnen M, Simola M, Malmberg H. Prevention of relapses

of nasal polyposis with intranasal triamcinolone acetonide after polyp surgery: a
prospective double-blind, placebo-controlled, randomised study with a 9-month
follow-up. Clin Otolaryngol. 2012 Apr. 37(2):117-23. [Medline].

9. Nguyen DT, Felix-Ravelo M, Arous F, Nguyen-Thi PL, Jankowski R. Facial

pain/headache before and after surgery in patients with nasal polyposis. Acta
Otolaryngol. 2015 Jun 25. 1-6. [Medline].
10. Brescia G, Marioni G, Franchella S, et al. A prospective investigation of predictive
parameters for post-surgical recurrences in sinonasal polyposis. Eur Arch
Otorhinolaryngol. 2015 Mar 13. [Medline].

11. Bhattacharyya N. Progress in surgical management of chronic rhinosinusitis and nasal

polyposis. Curr Allergy Asthma Rep. June 2007. 3:216-20. [Medline].

12. Garrel R, Gardiner Q, Khudjadze M, Demoly P, Vergnes C, Makeieff M. Endoscopic

surgical treatment of sinonasal polyposis-medium term outcomes (mean follow-up of
5 years). Rhinology. 2003 Jun. 41(2):91-6. [Medline].

13. Gosepath J, Mann WJ. Current concepts in therapy of chronic rhinosinusitis and nasal
polyposis. ORL J Otorhinolaryngol Relat Spec. 2005. 67(3):125-36. [Medline].

14. Mostafa BE, Abdel Hay H, Mohammed HE, Yamani M. Role of leukotriene
inhibitors in the postoperative management of nasal polyps. ORL J Otorhinolaryngol
Relat Spec. 2005. 67(3):148-53. [Medline].
Nasopharyngeal Stenosis


The nasopharynx is defined as the superior portion of the pharynx that lies between the
choanae of the nasal cavity and the oropharynx (ie, the level of the posterior limit of the soft
palate). Stenoses of this area are rare. They are classified according to their etiology, which
may be primary (ie, due to a disease process) or secondary (ie, iatrogenic). However, most
current cases are understood to be secondary to tonsillectomy, adenoidectomy,
uvulopalatoplasty, or radiotherapy for nasopharyngeal carcinoma.

Because of a high incidence of recurrence, the treatment of this condition is challenging.

Even with optimal planning and surgical technique, many patients require repeat operations
to obtain a satisfactory result. Therefore, many treatment modalities are being tried to cure
this problem.

Nasopharyngeal stenosis (NPS) should not be confused with choanal atresia. Choanal atresia
is a congenital deformity that causes a narrow or completely obstructed airway at the choanae
that often extends into the nasal cavity. Generally, choanal atresia includes a bony
component. Conversely, nasopharyngeal stenosis (NPS), by definition, is outside of the nasal
cavity, is not congenital, and is caused by scar tissue secondary to a disease process or
traumatic insult.

An image depicting complete nasopharyngeal stenosis can be seen below.

Complete nasopharyngeal stenosis.

History of the Procedure

Historically, many procedures have been used in an attempt to correct nasopharyngeal

stenosis (NPS).

Simple dilatation is generally not successful except in mild partial occlusion.

A seton technique has been used with limited success. A heavy silk suture or other
seton material is put in place, and, as it passes through the scar tissue, epithelialization
of the tract develops. This tract can then be divided with the hope that the
epithelialization prevents the stenosis from recurring.

One reportedly successful technique involves division of the obstruction and resection
of the scar tissue, using a stent to maintain the opening. The principle is similar to that
used in correction of choanal atresia. Many variations of this procedure have been
performed, including one in which a split-thickness graft is used to help resurface the
raw areas.

One of the most successful methods of repair is division of the obstruction and
resection of the scar tissue along with resurfacing using rotational mucosal flaps.

Since 2008, endoscopic transnasal repair using either powered shavers or lasers has
become a popular method of repairing nasopharyngeal stenosis.

Endoscopic transnasal CO 2 laser ablation of the stenosis followed by balloon dilation

and mitomycin application has been reported. [1]


Patients with nasopharyngeal stenosis could frequently suffer from other significant
morbidities like phonatory changes, sleep disordered breathing and otologic disturbances e.g.
secretory otitis media and hearing loss.[2, 3, 4]



Nasopharyngeal stenosis (NPS) is relatively rare. The true incidence of this rare condition is
difficult to assess. In 1944, in a 10-year review of 100,000 tonsillectomies and
adenoidectomies at the Manhattan Eye, Ear, and Throat Hospital, Imperatori found only 3
cases.[5] This condition has no sex predilection.


Most cases of nasopharyngeal stenosis (NPS) are caused by inexpert surgery and postsurgical
scarring. Overly enthusiastic adenoidectomies or uvulopalatoplasties are the usual operations
that lead to nasopharyngeal stenosis (NPS). However, tonsillectomies, surgery of the soft
palate, and pharyngeal surgeries to treat velopharyngeal incompetence can also cause
nasopharyngeal stenosis (NPS). The literature prior to 1929 reports that most cases were due
to the gumma of tertiary syphilis of the mouth, pharynx, and palate and the treatment of these
lesions with caustic chemicals.

Giannoni et al (1998) have reported 9 cases of nasopharyngeal stenosis in children following

adenoidectomy with KTP Laser. Many reports have been published of nasopharyngeal
stenosis following radiotherapy for nasopharyngeal carcinoma.[6, 7, 8, 2, 9] Other rare causes in
the literature include rhinoscleroma, lupus, diphtheria, scarlet fever, bullous pemphigoid,
tuberculosis, and acid burns.


Nasopharyngeal stenosis (NPS) may appear months to years after adenoidectomy or

uvuloplasty or radiotherapy. It results from excess mucosal removal or scarring during
surgery or radiotherapy followed by scar contracture and maturation. The degree and extent
of the stenosis may vary from patient to patient. The scar tissue may cause a circumferential
narrowing, a web, or bands. A discrete circumferential web or a long stenosed segment that
forms a narrow tunnel several centimeters long may be present.


The severity of symptoms is related to the degree of nasopharyngeal stenosis (NPS). The
history includes a traumatic insult (iatrogenic, traumatic, or infective) to the nasopharynx.
Symptoms include mouth breathing, snoring, rhinorrhea, hyponasality, dysphagia, otalgia,
loss of hearing (otitis media), and anosmia. If these symptoms develop following a surgical
procedure in the nasopharynx or radiotherapy, nasopharyngeal stenosis (NPS) should be
Upon examination, the mucosa of the nasal airway may be blue and boggy, as is seen with
nasal obstruction. Airflow through the nostrils may be reduced or eliminated. Scar tissue that
involves the soft palate and tonsil pillars may be visible. A postnasal mirror or a rigid or
flexible nasendoscope aids in making the stenosis visible.


The severity of the symptoms must be balanced against the difficulty of surgical repair and
the possibility of recurrence and multiple operations. Many patients are young and have to
live with potentially progressive symptoms for many years. Symptoms are usually severe at
presentation, and surgical intervention is usually required.

Relevant Anatomy

The nasopharynx can be thought of as an essentially cuboidal space. The roof is formed by
the base of the skull and the sphenoid sinus, anteriorly bounded by the choanae and posterior
portion of the vomer. The floor consists of the superior surface of the soft palate and uvula.
Incorporated into the lateral walls are the eustachian tube orifices and the Rosenmller
fossae. The posterior wall is the superior extension of the posterior pharyngeal wall.

The mucosa of the nasopharynx is the respiratory type. The midline usually contains a large
deposit of lymphoid tissue that often extends into the Rosenmller fossae.

The shape of the nasopharynx changes with respiration and deglutition. During respiration,
the soft palate is drawn away from the posterior pharyngeal wall to open an airway. During
deglutition, the palate elevates and contacts the nasopharynx so that food and fluid do not
pass into the nose.


Surgical correction of nasopharyngeal stenosis (NPS) may be contraindicated in the presence

of the patient's comorbidities and inability to tolerate anesthesia or surgery, but the
symptoms, which are usually severe at presentation, usually require surgical intervention.


Imaging Studies
CT scanning and virtual endoscopy of the nasopharyngeal region can enable diagnosis and
proper evaluation of the degree and extent of stenosis. This can, in turn, help to plan the
surgical treatment. Axial CT scans can accurately define the nature and thickness of the
atresia, the narrowing of the posterior nasal cavity, and the thickening of the vomer. A
thorough preoperative assessment is needed to ensure the best surgical option for the
individual lesion.

Diagnostic Procedures

Preoperative rigid nasal endoscopic examination and/or flexible nasopharyngolaryngoscopy

is essential to assess the thickness, nature and extent of the stenosis, the deformity of the
posterolateral aspect of the nasal cavity, and to identify anatomical deformities at the level of
the vomer and the posterior nasal cavity. Identifying concurrent upper aerodigestive tract
stenosis, which may be present, is important.

Histologic Findings

Histology of the resected scar tissue from the stenotic segment usually reveals respiratory
epithelial lined stromal tissue with chronic inflammation, edema, and fibrosis.


Krespi and Kacker proposed the following scale to grade the severity of nasopharyngeal

Nasopharyngeal stenosis (NPS) type I (mild)

Nasopharyngeal stenosis (NPS) type II (moderate)

Nasopharyngeal stenosis (NPS) type III (severe, wherein the entire palate fuses with
the posterior and lateral palatal wall, leaving a residual nasopharynx opening with a
diameter of less than 1 cm.)

Wang et al (2009) have divided acquired nasopharyngeal stenosis based on the duration
between causative trauma/radiotherapy and diagnosis into the following 3 types:[11]

Type 1 - Diagnosed within 3 months of causative trauma/radiotherapy

Type 2 - Diagnosed between 3-6 months of causative trauma/radiotherapy

Type 3 - Diagnosed more than 6 months after trauma or radiotherapy

Treatment & Management

Medical Therapy

Nasopharyngeal stenoses (NPS) are typically challenging to correct and often recur.
Prevention is the best form of treatment. Careful operative technique, judicious use of
electrocautery, and adequate preoperative evaluation for adenoidectomy or uvulopalatoplasty
during the primary surgery are essential to prevent nasopharyngeal stenosis (NPS). In cases
of mild scarring, McLaughlin et al found some success with triamcinolone acetonide
injections, but the only curative treatments for acquired nasopharyngeal stenosis (NPS) are

Surgical Therapy

A thorough preoperative assessment of the lesion is needed to ensure that the best surgical
option for the individual lesion is used.Nasopharyngeal stenosis rarely exists in isolation.
Often concurrent stenosis of the upper aerodigestive tract may require general anesthesia for

Many surgical approaches have been suggested for nasopharyngeal stenosis, including
transnasal, transpalatal, transantral, sublabial transnasal endoscopic, and transseptal
approaches.[2, 7, 8] The transpalatal approach offers excellent exposure and a high success rate
but is time consuming and may be associated with bleeding and sequelae like palatal muscle
dysfunction, palatal fistula, and maxillofacial disturbances.[13] The transnasal approach
provides narrow exposure, making raising of the mucosal flaps difficult. Also, injury to the
eustachian tube and the skull base is possible.[14]

Other surgical options include steroid injections, scar lysis with CO2 laser, plasma hook,
yttrium-aluminum-garnet (YAG) laser,[2] or with power instruments like shavers, Surgitron
high-frequency radio waves,[15] skin grafts, Z-plasty repair, various local mucosal flaps,
insertion of prosthetic stents, silastic grommets, nasopharyngeal obturators, and topical
application of mitomycin C and balloon dilation of the stenotic segment.[1, 16, 17]
Bivalved palatal transposition flap

Described by Toh et al in 2000, this procedure is performed with the patient under general
anesthesia with orotracheal intubation.[18] The patient is supine with the neck extended. A
mouth gag is used to expose the oropharynx. Local anesthetic (1% lidocaine) with adrenaline
(1:100,000) is infiltrated into the operative site. A transverse and slightly curvilinear incision
is marked out on either side of the stenosis. This incision is extended inferolaterally to the
expected position of the base of the posterior tonsillar pillars.

The stenosis is then bivalved by elevating mucosal flaps on a submucosal plane off the oral
and nasopharyngeal surfaces of the soft palate. The superiorly based flap represents the
nasopharyngeal surface of the soft palate, and the inferiorly based flap from the
oropharyngeal side is attached to the posterior pharyngeal wall. The posterior half of the
bivalved palate is then transposed anteriorly and sutured to the incision on the oral side of the
soft palate. The inferiorly based mucosal flap is transposed superiorly and sutured to the
denuded portion of the posterior pharyngeal wall.

Laterally based pharyngeal flap

For this procedure, as described by Cotton in 1985, the patient is anesthetized and local
anesthetic and adrenaline are infiltrated, as in the bivalved palatal transposition flap.[19] A
lateral incision is made through the scar tissue into the lateral pharyngeal wall. The incision is
deepened as far as possible without damaging important structures in the parapharyngeal
space. The mucosa is now elevated to allow a considerable amount of scar tissue removal.
The entire posterior pharyngeal wall is elevated as a laterally based pharyngeal flap (thus,
only one side of the nasopharyngeal stenosis is dissected).

The laterally based pharyngeal flap is elevated as a mucomuscular flap at the plane of the
prevertebral fascia. The inferior limit of the flap is dissected as far back as possible. The
inferior limit of the flap is dissected as far back as possible, and the pharyngeal
mucomuscular flap is mobilized and sewn into position, covering the denuded area of the
lateral walls of the nasopharynx and oropharynx. Smith has used sternocleidomastoid
myocutaneous flap reconstruction for nasopharyngeal stenosis (NPS).[20]

Carbon dioxide laser

Krespi and Kacker have reported on the largest number of patients who have undergone
successful nasopharyngeal stenosis (NPS) correction with a CO2 laser.[10] After scar tissue
was excised with the laser, patients with moderate-to-severe stenosis received a
nasopharyngeal obturator to be worn at night for 2-6 months to prevent restenosis. The CO2
laser was reported to cause less thermal damage to adjacent tissue and minimal mucosal de-
epithelialization, and it offered better hemostasis.

Jones et al used a CO2 laser under general anesthesia to create an opening in the
nasopharynx.[3] The patients were then fitted with removable and adjustable palatal obturators
to keep the nasopharynx open. A daytime insert piece with a small obturator hole for
diminished velopharyngeal insufficiency and a night-time piece without an insert to
maximize recumbent airflow were also used. The obturators were removed after 6 months,
and a topical application of mitomycin C was used as a fibroblast inhibitor. These authors
monitored their patients with polysomnography and have reported satisfactory results.

Igwe et al and Sidell et al report the use of a flexible CO2 laser fiber through the working
channel of a nasal endoscope to make radial incisions on the stenosis under direct
visualization.[1, 16]
The laser is then removed and a controlled radial expansion balloon
dilation device is inserted, advanced to span the stenotic segment and inflated to achieve
adequate dilation. Mitomycin-C is then topically applied to the area of dilation. They report
successful long lasting dilation without complications with a follow-up period of 12-18

Plasma hook

Madgy et al treated 3 cases of severe nasopharyngeal stenosis (NPS) with plasma

radiofrequencybased coblation.[4] A crescent of scar tissue was excised with the plasma
hook. The crescent extended approximately 5 mm laterally to each side and approximately 5
mm posteriorly to the pharyngeal wall. In one case, they applied mitomycin C to the raw
edges to reduce scarring and recurrence. They reported that the plasma hook excision incurs
less epithelial damage and produces a smaller area of collagen denaturation than conventional
electrocautery. In addition, the procedure itself is easy to perform and offers satisfactory

Eppley et al compared the use of (1) preoperatively fabricated stents made from a clasped
palatal appliance onto which hollow acrylic conduits were extended through surgically re-
created pharyngeal ports with (2) intraoperatively fashioned silastic grommets.[21] They found
that the palatal stents were less tolerated than the silastic grommets. In addition, the grommet
stent obviates the need for extensive preoperative preparation and is easy to insert and
remove; also, during the stenting, an exchange of air occurs. Patient tolerance was found to
be better with the grommet stents, which could, therefore, be retained longer with better

Transnasal endoscopic repair

The advantages of this method are that it offers a good vision of the operative field and
enables accurate removal of the stenotic plate without damaging neighboring structures,
thereby reducing the incidence of re-stenosis. This is a safe procedure with minimal blood
loss, rapid recovery, and short hospitalization. During follow-up, remove postoperative
granulations or polyps at the site of the neochoana.[9]

Ku et al in 2007 described transnasal endoscopic YAG laser resection of posterior choanal

stenosis following radiotherapy for nasopharyngeal carcinoma in 5 patients.[8] All 5 were
symptom free postoperatively, although 2 developed mild re-stenosis not requiring surgery.
In 2008, Wang et al described successful transnasal endoscopic repair without postoperative
stenting in 18 out of 19 patients with nasopharyngeal stenosis (NPS) following radiotherapy
for nasopharyngeal carcinoma. One patient required revision surgery.[9]

Wang et al (2009) used temperature controlled radiofrequency repair (TCRF) with the aid of
an endoscope in 32 patients. All patients with type 1 and 2 received silicon stents. Three
patients required revision of the procedure, and one patient required a third revision, which
was performed via transpalatal approach. They found that the technique worked best in those
patients who were diagnosed more than 3 months after trauma/radiotherapy (ie, type 2 and
type 3 cases).

Hussein et al (2013)[15] have described the use of Surgitron high-frequency radio waves to
remove scar tissue, followed by application of mitomycin C to the wound and then placement
of stents for 2 weeks.

Intraoperative Details

Three methods of repair are described below.

Bivalved palatal transposition flap

Described by Toh et al in 2000, this procedure is performed with the patient under general
anesthesia with orotracheal intubation. The patient is supine with the neck extended.[18] A
mouth gag is used to expose the oropharynx. Local anesthetic (1% lidocaine) with adrenaline
(1:100,000) is infiltrated into the operative site. A transverse and slightly curvilinear incision
is marked out on either side of the stenosis. This incision is extended inferolaterally to the
expected position of the base of the posterior tonsillar pillars.

The stenosis is then bivalved by elevating mucosal flaps on a submucosal plane off the oral
and nasopharyngeal surfaces of the soft palate. The superiorly based flap represents the
nasopharyngeal surface of the soft palate, and the inferiorly based flap from the
oropharyngeal side is attached to the posterior pharyngeal wall. The posterior half of the
bivalved palate is then transposed anteriorly and sutured to the incision on the oral side of the
soft palate. The inferiorly based mucosal flap is transposed superiorly and sutured to the
denuded portion of the posterior pharyngeal wall.

Laterally based pharyngeal flap

For this procedure, as described by Cotton in 1985, the patient is anesthetized and local
anesthetic and adrenaline are infiltrated as for the bivalved palatal transposition flap.[19] A
lateral incision is made through the scar tissue into the lateral pharyngeal wall. The incision is
deepened as far as possible without damaging important structures in the parapharyngeal

The mucosa is now elevated to allow a considerable amount of scar tissue removal. The
entire posterior pharyngeal wall is elevated as a laterally based pharyngeal flap (thus, only
one side of the nasopharyngeal stenosis is dissected). The laterally based pharyngeal flap is
elevated as a mucomuscular flap at the plane of the prevertebral fascia. The inferior limit of
the flap is dissected as far back as possible. A back-cut is now performed inferiorly to
mobilize the pharyngeal flap. This mucomuscular flap is mobilized and sewn into position,
covering the denuded area of the lateral walls of the nasopharynx and oropharynx.

Palatal eversion

AbdelFattah described this procedure for patients who develop nasopharyngeal stenosis
following adenotonsillectomy. The soft palate is divided in the midline. The fibrous tissue
causing stenosis is removed, followed by eversion and fixation of the two palatal divisions on
either side for 6 weeks to allow complete epithelialization of the stenotic area, followed by
another operation to reunite the soft palate in the midline.[22]

Transnasal endoscopic repair

This procedure is performed under general anesthesia, as described by Wang et al.[9] The nose
is decongested using pledgets soaked in a solution of 1% lidocaine hydrochloride and 0.25%
phenylepinephrine. A solution of 1% lidocaine hydrochloride with 1:100,000 epinephrine is
administered with a spinal needle to the stenotic portion and posterior septum under direct
visualization using the 4mm 0 rigid telescope.

Under endoscopic visualization, a flaps knife is used to trim the scarred mucosa in the
posterior choanae. Additional scar tissue at the posterior end of the inferior or middle
turbinate can be excised with a powered shaver or Blakesley forceps. Ku et al have used the
YAG laser to remove the scar tissue under endoscopic vision.[8] Hussein et al[15] have
described the use of Surgitron high-frequency radio waves to remove the scar tissue, followed
by application of mitomycin C and stenting for 2 weeks. Care is taken to avoid damage to the
normal nasal mucosa. Tissue is also taken for histopathology to rule out recurrence of
carcinoma in cases of stenosis following radiotherapy for nasopharyngeal carcinoma. After
the surgical procedure, some authors used Merocel as a stent,[8] while others did not use any
stents.[9] At the follow-up visit, an endoscopic examination is performed and any granulation
tissue or polyps at the site of the neochoana are removed.

Postoperative Details

A nasopharyngeal tube is left in for 24-48 hours to allow the flap to settle, to maintain an
airway, and to help with suctioning. The patient is maintained on clear fluids for up to a
week. Postoperative antibiotics are used. The stents are removed 2-6 weeks after surgery,
depending on the surgeon. The patients are advised to perform nasal douching with normal
saline and steroid nasal sprays.


Monitor the patient with a rigid nasal endoscope to check that the surgery is successful and
the patient has no complications. In the long-term, polysomnography and nasal endoscopy
help to monitor for restenosis.

Postoperative airway problems and hemorrhage have not been reported. Velopharyngeal
reflux has been reported but is transient and gradually resolves. The main complication is re-
stenosis. This condition is common, and the literature suggests that a repeat operation is
performed in 10-20% of patients.

Outcome and Prognosis

Even with optimal planning and surgical technique, many patients require repeat operations
to obtain a satisfactory result. Giannoni et al showed that acquired nasopharyngeal stenosis
(NPS) symptoms had an average onset time of 3.1 weeks postsurgery.[23] Stepnick reported
recurrent scarring and stenosis within 6 weeks of treating nasopharyngeal stenosis (NPS) with
the placement of a free flap.[24] Ku et al have reported nasopharyngeal stenosis (NPS)
symptoms developing an average of 10.5 months (range 2-40 months) postradiation in
patients who have nasopharyngeal carcinoma.[7]

Future and Controversies

Since the discovery and widespread use of antibiotics, the incidence of nasopharyngeal
stenosis (NPS) has declined. The main etiologies in current practice include tonsillectomy,
adenoidectomy, velopharyngeal surgery, uvulopalatopharyngoplasty, and postradiotherapy
cases of nasopharyngeal carcinoma.

The nature of the stenosis renders it difficult to treat successfully. This, coupled with its
rarity, leaves most surgeons with limited experience in the condition. Mucosal flaps of the
palate and pharynx were the most successful techniques for repair. However, the advent of
the rigid nasal endoscope, powered shavers, and lasers has made it easier to diagnose, operate
under direct vision with minimal hospital stay, and monitor the patient postoperatively.

1. Sidell D, Chhetri DK. CO2 laser ablation and balloon dilation for acquired
nasopharyngeal stenosis: a novel technique. Laryngoscope. 2011 Jul. 121(7):1486-9.

2. Shepard PM, Houser SM. Choanal stenosis: an unusual late complication of radiation
therapy for nasopharyngeal carcinoma. Am J Rhinol. 2005 Jan-Feb. 19(1):105-8.

3. Jones LM, Guillory VL, Mair EA. Total nasopharyngeal stenosis: treatment with laser
excision, nasopharyngeal obturators, and topical mitomycin-c. Otolaryngol Head
Neck Surg. 2005 Nov. 133(5):795-8. [Medline].

4. Madgy DN, Belenky W, Dunkley B, Shinhar S. A simple surgical technique using the
plasma hook for correcting acquired nasopharyngeal stenosis. Laryngoscope. 2005
Feb. 115(2):370-2. [Medline].

5. Imperatori CJ. Atresia of the pharynx operated upon by the MacKenty method. Arch
Otol Rhinol Laryngol. 1944. 53:329-34.

6. Bonfils P, de Preobrajenski N, Florent A, Bensimon JL. [Choanal stenosis: a rare

complication of radiotherapy for nasopharyngeal carcinoma]. Cancer Radiother. 2007
May. 11(3):143-5. [Medline].

7. Ku PK, Tong MC, Tsang SS, van Hasselt A. Acquired posterior choanal stenosis and
atresia: management of this unusual complication after radiotherapy for
nasopharyngeal carcinoma. Am J Otolaryngol. 2001 Jul-Aug. 22(4):225-9. [Medline].

8. Ku PK, Tong MC, van Hasselt A. Application of holmium yttrium aluminium garnet
(YAG) laser in treatment of acquired posterior choanal atresia following radiotherapy
for nasopharyngeal carcinoma. J Laryngol Otol. 2007 Feb. 121(2):138-42. [Medline].

9. Wang QY, Wang SQ, Lin S, Chen HH, Lu YY. Transnasal endoscopic repair of
acquired posterior choanal stenosis and atresia. Chin Med J (Engl). 2008 Jun 20.
121(12):1101-4. [Medline].
10. Krespi YP, Kacker A. Management of nasopharyngeal stenosis after
uvulopalatoplasty. Otolaryngol Head Neck Surg. 2000 Dec. 123(6):692-5. [Medline].

11. Wang QY, Chai L, Wang SQ, Zhou SH, Lu YY. Repair of acquired posterior choanal
stenosis and atresia by temperature-controlled radio frequency with the aid of an
endoscope. Arch Otolaryngol Head Neck Surg. 2009 May. 135(5):462-6. [Medline].

12. McLaughlin KE, Jacobs IN, Todd NW, Gussack GS, Carlson G. Management of
nasopharyngeal and oropharyngeal stenosis in children. Laryngoscope. 1997 Oct.
107(10):1322-31. [Medline].

13. Brown OE, Pownell P, Manning SC. Choanal atresia: a new anatomic classification
and clinical management applications. Laryngoscope. 1996 Jan. 106(1 Pt 1):97-101.

14. Morgan DW, Bailey CM. Current management of choanal atresia. Int J Pediatr
Otorhinolaryngol. 1990 Mar. 19(1):1-13. [Medline].

15. Hussein J, Tan TS, Chong AW, Narayanan P, Omar R. Velopharyngeal and choanal
stenosis after radiotherapy for nasopharyngeal carcinoma. Auris Nasus Larynx. 2013
Jun. 40(3):323-6. [Medline].

16. Igwe CN, Sharma R, Roberts D, Hopkins C. Use of balloon dilatation as an adjunctive
treatment for complete nasopharyngeal stenosis: a technical innovation. Clin
Otolaryngol. 2012 Feb. 37(1):88-9. [Medline].

17. Chheda NN, Postma GN. Balloon dilation of an acquired nasopharyngeal stenosis.
Otolaryngol Head Neck Surg. 2009 Jun. 140(6):939-41. [Medline].

18. Toh E, Pearl AW, Genden EM, Lawson W, Urken ML. Bivalved palatal transposition
flaps for the correction of acquired nasopharyngeal stenosis. Am J Rhinol. 2000 May-
Jun. 14(3):199-204. [Medline].

19. Cotton RT. Nasopharyngeal stenosis. Arch Otolaryngol. 1985 Mar. 111(3):146-8.

20. Smith ME. Prevention and treatment of nasopharyngeal stenosis: Operative

Techniques in Otolaryngology - Head and Neck Surgery. 2005. Vol. 16, Issue 4:242-
21. Eppley BL, Sadove AM, Hennon D, van Aalst JA. Treatment of nasopharyngeal
stenosis by prosthetic hollow stents: Clinical experience in eight patients. Cleft Palate
Craniofac J. 2006 May. 43(3):374-8. [Medline].

22. Abdel-Fattah G. Palatal eversion: A new technique in treatment of nasopharyngeal

stenosis. Int J Pediatr Otorhinolaryngol. 2012 Mar 21. [Medline].

23. Giannoni C, Sulek M, Friedman EM, Duncan NO 3rd. Acquired nasopharyngeal

stenosis: a warning and review. Arch Otolaryngol Head Neck Surg. 1998 Feb.
124(2):163-7. [Medline].

24. Stepnick DW. Management of total nasopharyngeal stenosis following UPPP. Ear
Nose Throat J. 1993 Jan. 72(1):86-90. [Medline].

25. Fairbanks DN. Operative techniques of uvulopalatopharyngoplasty. Ear Nose Throat

J. 1999 Nov. 78(11):846-50. [Medline].

26. Hanson RD, Olsen KD, Rogers RS 3rd. Upper aerodigestive tract manifestations of
cicatricial pemphigoid. Ann Otol Rhinol Laryngol. 1988 Sep-Oct. 97(5 Pt 1):493-9.

27. Johnson LB, Elluru RG, Myer CM 3rd. Complications of adenotonsillectomy.

Laryngoscope. 2002 Aug. 112(8 Pt 2 Suppl 100):35-6. [Medline].

28. Stevenson EW. Cicatricial stenosis of the nasopharynx. A comprehensive review.

Laryngoscope. 1969 Dec. 79(12):2035-67. [Medline].

29. Van Duyne J, Coleman JA Jr. Treatment of nasopharyngeal inlet stenosis following
uvulopalatopharyngoplasty with the CO2 laser. Laryngoscope. 1995 Sep. 105(9 Pt
1):914-8. [Medline].
Nonsurgical Treatment of Nasal Polyps


Nasal polyposis is an inflammatory condition of unknown etiology. Nasal polyps are the most
common tumors of the nasal cavity. Approximately 30% of patients with nasal polyps test
positive for environmental allergies. The prevalence of nasal polyps is increased in children
with cystic fibrosis and persons with known aspirin hypersensitivity. Nasal polyposis can
impair a person's quality of life more than perennial allergic rhinitis. Olfaction and nasal
obstruction are the most important considerations in terms of symptoms.


Nasal polyposis results from chronic inflammation of the nasal and sinus mucous
membranes. Chronic inflammation causes a reactive hyperplasia of the intranasal mucosal
membrane, which results in the formation of polyps. The precise mechanism of polyp
formation is incompletely understood.

In 1990, Tos reported 10 pathogenic theories of nasal polyp formation:[1]

Adenoma and fibroma theories

Necrosing ethmoiditis theory

Glandular cyst theory

Mucosal exudate theory

Cystic dilatation of the excretory duct and vessel obstruction theory

Blockade theory

Periphlebitis and perilymphangitis theory

Glandular hyperplasia theory

Gland new formation theory

Ion transport theory

Multiple chemical mediators have been identified in nasal polyps but their significance has
not been completely elucidated. Some of these mediators may be released by the polyps
themselves and others by the eosinophils found in certain subsets of polyps. Cysteinyl
leukotriene receptors and interleukin-5 (IL-5) appear to be the most well studied.



United States

Nasal polyps are present in 5% of nonallergic people and only 1.5% of people with allergic
rhinitis. No racial or sexual predilection is reported. The prevalence is increased in patients
with cystic fibrosis and aspirin-hypersensitivity triad.


Morbidity from polyps is directly related to their location and size.

Obstruction of the sinus ostia frequently occurs and may lead to acute or chronic sinus
conditions. With increased growth, polyps can cause bony destruction because they
can exert pressure on bone. Polyps may cause destruction of the nasal bones or other
facial bones.

Nasal obstruction due to polyposis can also lead to hyposmia or even anosmia.

Nasal polyps are not known to be premalignant. However, they may be confused with
papillomas, including inverting papillomas, which are known to be precursors of
malignant lesions. In addition, polyps can sometimes arise from inflammation caused
by malignant or premalignant nasal lesions. These polyps can obstruct visualization of
the more concerning lesions and sometimes cause delay in diagnosis.

Clinical Presentation


Patients with massive nasal polyposis typically present with increasing nasal congestion,
hyposmia to anosmia, changes in sense of taste, and persistent postnasal drainage. Headaches
and facial pain and discomfort are not uncommon and are found in the periorbital and
maxillary regions. On occasion, a patient with completely obstructing nasal polyposis
presents with symptoms of obstructive sleep apnea.
Patients with solitary polyps frequently present with only symptoms of nasal obstruction,
which may change with a shift in position. For example, while lying supine, the polyp may
swing posteriorly, opening up the nasal cavity. In an upright position, the polyp has a more
obstructive effect.

Whether 1 or more polyps are present, patients may have symptoms of acute, recurrent, or
chronic rhinosinusitis if the polyps obstruct the sinus ostia.


Intranasal examination reveals a fleshy translucent mass or masses in the nasal cavity, usually
originating in the superior nasal vault. Polyps can be observed originating in the ethmoid
region, from the maxillary sinus ostium (antral choanal polyps), the turbinates, or the septum.
Obstructing polyps may make thorough intranasal examination difficult. See the images

Nasal polyposis, right nasal passage.

Nasal polyposis, right nasal passage.

Mucopurulent discharge occasionally emanate from the ethmoid region or the superior nasal
vault, suggesting an underlying rhinosinusitis. Septal deformities may make the examination
more difficult.


See the list below:


Chronic sinusitis

Chronic inflammation of indeterminate etiology

Differential Diagnoses

Diagnostic Considerations

Inverting papilloma is another condition to consider in the differential diagnosis.

Differential Diagnoses

Allergic Rhinitis in Otolaryngology and Facial Plastic Surgery

Juvenile Nasopharyngeal Angiofibroma

Malignant Tumors of the Nasal Cavity

Turbinate Dysfunction

Laboratory Studies

See the list below:

Allergy testing in patients who have polyps and are not clinically allergic is

o Many clinicians think that the expense is not justified.

o On the contrary, a thorough allergy evaluation should be considered in patients

with a history of environmental allergies or a strong family history of

Children who present with nasal polyposis should be tested for cystic fibrosis with
either a sweat chloride test or with hematologic genetic testing.

Imaging Studies

See the list below:

Coronal sinus CT is the imaging study of choice in the evaluation of patients with
nasal polyposis.

o Coronal CT of the paranasal sinuses is best for delineating the underlying

pathology, the extent of disease, and possible bony destruction.

o Nonenhanced CT with 2- to 3-mm sections helps to delineate the location and

origin of the visible polyps, evaluate the underlying condition of all of the
sinuses, and assess the anatomy of the paranasal sinuses in the event of
surgical intervention.

MRI is not an appropriate imaging modality for nasal polyposis unless intracranial
extension is suspected. Bony details of the paranasal sinus anatomy are poorly
visualized on MRI.
Radiography with Waters views may show opacification of the sinuses.


Nasal endoscopy in an office setting can sometimes be helpful in the diagnosis and evaluation
of nasal polyps. This technique helps illuminate and improves visualization of the dark
recesses of the nasal cavity. Endoscopy may allow the examiner to see beyond an obstructing
nasal septal deviation, an enlarged turbinate, or an obstructing polyp.

Histologic Findings

Biopsy is not always required for the diagnosis of nasal polyps. Nasal masses that do not
have the classic appearance of bilateral nasal polyps or that do not respond to conservative
treatment should be examined with careful biopsy for diagnosis. The histologic appearance of
nasal polyps varies from edematous tissue with a few glands to an increase in glandular
elements. Eosinophils may be present, indicating an allergic component.

Many factors play a role in the formation of nasal polyp. Epithelial damage has been
implicated in the pathogenesis of polyps. Epithelial cells can undergo activation in response
to allergens, pollutants, and infectious agents. The cells release various factors that play a role
in the inflammatory response and subsequent repair. The epithelium of nasal polyps shows
goblet cell hyperplasia and mucous hypersecretion that may play a role in nasal obstruction
and rhinorrhea.

Mucin synthesis and goblet cell hyperplasia are thought to be under control of epidermal
growth factors (EGF). Inhibitors may block mucous production and goblet cell hyperplasia.
Free radicals are highly reactive molecules with an unpaired electron in the outer orbit and
may also play a role in polyp formation. The body produces endogenous oxidants as a result
of the leakage of electrons from electron transport chains, phagocytic cells and endogenous
enzyme systems (MAO, P450, etc).

Exogenous factors include radiation, air pollutants, tobacco smoke, sun exposure, ozone, and
others. A certain physiologic level of reactive oxygen species is necessary for proper
regulation of cell functions. Exposure to oxidants can initiate free radical-mediated reactions
and lead to oxidative stress. Free radicals can result in cellular damage or death and
subsequent tissue damage.
Several inflammatory factors have been isolated and are proven to be expressed by nasal
polyps. These factors include endothelial vascular cell adhesion molecule (VCAM)-1, nitric
oxide synthase, granulocyte-macrophage colonystimulating factor (GM-CSF), eosinophil
survival enhancing activity (ESEA), cys-leukotrienes (Cys-LT) and many other cytokines.

Treatment & Management

Medical Care

The management of nasal polyps should be based on the causative factors. Unfortunately,
most cases of nasal polyps have an unclear etiology. Even if the patient is allergic, no clinical
evidence shows that the management of allergies reduces or eliminates polyps. Because the
underlying etiology in most cases is inflammatory, medical management is aimed at
nonspecific treatment of this inflammatory disorder.

Oral corticosteroids are the most effective medical treatment for nasal polyps.[3, 4, 5]
nonspecific anti-inflammatory agent quickly and substantially reduces the size of
inflammatory polyps and improves symptoms. Patients whose polyps respond to oral
corticosteroids may be re-treated safely 3-4 times a year, especially if they are not candidates
for surgery. The mechanism of action of corticosteroids is unclear. One study showed that
corticosteroids induce apoptosis in inflammatory cells in human nasal polyps in vitro.

Intranasal steroid sprays may reduce or retard the growth of small nasal polyps, but they are
relatively ineffective in massive nasal polyposis. Intranasal corticosteroid sprays reduce the
growth of small intranasal polyps and are most effective in the postoperative period to
prevent or retard regrowth of the polyps.

Rudmik et al conducted a meta-analysis that reviewed the effect of topical steroids (low-dose
administration methodology) on symptoms in patients with nasal polyps. Results suggest
topical nasal steroid therapy improves nasal symptoms in patients with chronic rhinosinusitis
and nasal polyposis. The study did not look specifically at the effect on polyp size or
regression, but rather only on whether or not the patients' symptoms improved. Readers
should be cautioned to recognize that since the studies reviewed did not measure polyp mass,
no statement can be made about the mechanisms underlying the observed symptomatic
improvements, as they may be due to improvement in associated rhinitis, rather than an effect
on the nasal polyps. In addition, most of the studies reviewed were from outside of North
Intrapolyp steroid injections have been shown to reduce polyp growth and nasal symptom
scores compared with intranasal medical therapy and appear to be a safe alternative to
surgery in select patients. More studies are necessary.[7]

A study by Moss et al indicated that although visual complications can occur following
steroid injections for nasal polyps, the likelihood is small. The study involved 78 patients
with chronic rhinitis or sinusitis who were treated with a total of 237 injections of
triamcinolone acetonide. The injections were either intraturbinate (152 injections) or
intrapolyp (85 injections). One patient experienced a visual change following an intrapolyp
injection, but it was transient and resolved spontaneously. The investigators also conducted a
review of nine case series encompassing a total of 117,669 intranasal steroid injections, of
which only three (0.003%) caused visual complications; all of these all resolved
spontaneously without permanent visual deficit.[8]

Leukotrienes are formed during the breakdown of arachidonic acid by the enzyme 5-
lipoxygenase. They are inflammatory mediators and have been implicated in the pathogenesis
of asthma, allergic rhinitis, and nasal polyposis. As a result, they have become targets for
therapeutic modulation. Early studies of leukotrienes synthesis inhibitors have shown
improvements in nasal airflow and reduction in nasal polyps on endoscopy and imaging
studies. Benefits appear to be greatest in patients with concomitant allergic rhinitis and
eosinophilic infiltration of the nasal polyps on histology.

Antifungal agents have no role in the management of nasal polyposis, but these agents may
be useful in cases of allergic fungal sinusitis with polyposis.

Other agents with a possible role in management of nasal polyposis are macrolides
antibiotics, topical diuretic therapy, and intranasal lysineacetylsalicylic acid.

Surgical Care

See Nasal Polyps, Surgical Treatment.


See the list below:

Consultation with an allergist is beneficial for patients with a history of environmental

Allergy pharmacotherapy or immunotherapy is beneficial for patients with allergy

Consultation with a pulmonologist is helpful for patients with lower airway allergy,
asthma, or cystic fibrosis.


Dietary modifications should be considered in patients with food allergy and nasal polyposis.
Controlling allergy in these patients is important, and recording a food diary or undergoing
tests for food allergy may help control symptoms and slow polyp growth.


Medication Summary

The only medications effective in shrinking polyps are corticosteroids. Available both orally
and topically, they provide a nonspecific anti-inflammatory response that reduces the size of
the polyps and improves symptoms related to nasal obstruction. Other medications currently
undergoing evaluation affect the nasal inflammatory pathway in different ways and
specificity, but they have not shown great promise.

Oral corticosteroids

Class Summary

The time-tested medical treatment for obstructing nasal polyps is oral corticosteroids. This
nonspecific anti-inflammatory agent significantly reduces the size of the inflammatory polyps
and improves symptoms quickly. Unfortunately, the effects are short lasting, and polyps
frequently regrow and cause similar symptoms within weeks to months.

Prednisone (Deltasone, Orasone)

Immunosuppressant to treat autoimmune disorders; may decrease inflammation by reversing

increased capillary permeability and suppressing PMN activity. Potent anti-inflammatory,
generically available, and cost effective.

Topical nasal corticosteroids

Class Summary
These induce a nonspecific anti-inflammatory response that should theoretically reduce the
size of polyps and prevent regrowth when used continuously. Available nasal steroid sprays
appear to be similarly effective and relatively safe for both short- and long-term use.

Fluticasone (Flonase)

Potent vasoconstrictive and anti-inflammatory activity; weak inhibitory potency on HPA

when applied topically. Advise patients to administer spray toward lateral nasal wall,
avoiding irritation to septum or having drug run down back of pharynx.

Mometasone (Nasonex)

Nasal spray; elicits anti-inflammatory activity. Indicated for nasal polyposis treatment.
Demonstrated no mineralocorticoid, androgenic, antiandrogenic, or estrogenic activity in
preclinical trials. Decreases rhinovirus-induced up-regulation in respiratory epithelial cells
and modulates pretranscriptional mechanisms. Reduces intraepithelial eosinophilia and
inflammatory cell infiltration (eg, eosinophils, lymphocytes, monocytes, neutrophils, plasma
cells). Before initial use, prime pump by actuating 10 times or until a fine spray appears; if
stored unused for > 1 wk, reprime. Advise patients to administer spray toward lateral nasal
wall, avoiding irritation to septum or having drug run down back of pharynx.

Budesonide inhaled (Rhinocort, Rhinocort Aqua)

Potent vasoconstrictive and anti-inflammatory activity. Budesonide is indicated for nasal

polyposis management. Advise patients to administer spray toward lateral nasal wall,
avoiding irritation to septum or having drug run down back of pharynx.

Leukotriene receptor antagonists

Class Summary

These agents prevent or reverse some of the pathologic features associated with the
inflammatory process mediated by leukotrienes.
Montelukast (Singulair)

Potent and selective antagonist of leukotriene D4 (LTD4) at the cysteinyl leukotriene

receptor, CysLT1. Prevents or reverses some of the pathologic features associated with the
inflammatory process mediated by leukotrienes C4, D4, and E4.


Further Outpatient Care

See the list below:

Patients with nasal polyposis can easily be monitored as outpatients, and they should
be examined by an otolaryngologist.

o Patients with limited symptoms may be monitored once or twice a year.

o Patients with severe obstructive symptoms may need closer follow-up,

especially if they are receiving high-dose oral corticosteroids or using nasal
steroid sprays long term.

Consider surgical intervention for nasal polyps after appropriate medical therapy is
unsuccessful and for patients with recurrent sinus infections that need treatment with
multiple antibiotics.


See the list below:


o Recurrent sinusitis

o Chronic sinusitis

o Acquired nasal deformity


o Proptosis

o Diplopia

o Meningitis

o Encephalitis


See the list below:

Medical therapy for nasal polyposis is usually reserved for patients who are not
surgical candidates or who require temporization of symptom relief.

Rarely do the polyps resolve, but they occasionally shrink enough to provide
symptomatic relief.

Patient Education

See the list below:

For excellent patient education resources, visit eMedicineHealth's Ear, Nose, and
Throat Center. Also, see eMedicineHealth's patient education article Sinus Infection.

1. Tos M. The pathogenic theories on the formation of nasal polyps. Am J Rhinol. 1990.

2. Bernstein JM, Gorfien J, Noble B. Role of allergy in nasal polyposis: a review.

Otolaryngol Head Neck Surg. 1995 Dec. 113(6):724-32. [Medline].

3. Van Zele T, Gevaert P, Holtappels G, Beule A, Wormald PJ, Mayr S, et al. Oral
steroids and doxycycline: two different approaches to treat nasal polyps. J Allergy
Clin Immunol. 2010 May. 125(5):1069-1076.e4. [Medline].

4. Martinez-Devesa P, Patiar S. Oral steroids for nasal polyps. Cochrane Database Syst
Rev. 2011 Jul 6. CD005232. [Medline].

5. Kirtsreesakul V, Wongsritrang K, Ruttanaphol S. Clinical efficacy of a short course of

systemic steroids in nasal polyposis. Rhinology. 2011 Dec. 49(5):525-32. [Medline].

6. Rudmik L, Schlosser RJ, Smith TL, Soler ZM. Impact of topical nasal steroid therapy
on symptoms of nasal polyposis: a meta-analysis. Laryngoscope. 2012 Jul.
122(7):1431-7. [Medline].

7. Becker SS, Rasamny JK, Han JK, Patrie J, Gross CW. Steroid injection for sinonasal
polyps: the University of Virginia experience. Am J Rhinol. 2007 Jan-Feb. 21(1):64-9.

8. Moss WJ, Kjos KB, Karnezis TT, et al. Intranasal steroid injections and blindness:
Our personal experience and a review of the past 60 years. Laryngoscope. 2014 Nov
6. [Medline].

9. Bikhazi NB. Contemporary management of nasal polyps. Otolaryngol Clin North Am.
2004 Apr. 37(2):327-37, vi. [Medline].

10. Burgel PR, Escudier E, Coste A, Dao-Pick T, Ueki IF, Takeyama K. Relation of
epidermal growth factor receptor expression to goblet cell hyperplasia in nasal polyps.
J Allergy Clin Immunol. 2000 Oct. 106(4):705-12. [Medline].
11. Dagli M, Eryilmaz A, Besler T, Akmansu H, Acar A, Korkmaz H. Role of free
radicals and antioxidants in nasal polyps. Laryngoscope. 2004 Jul. 114(7):1200-3.

12. Hamilos DL, Thawley SE, Kramper MA, Kamil A, Hamid QA. Effect of intranasal
fluticasone on cellular infiltration, endothelial adhesion molecule expression, and
proinflammatory cytokine mRNA in nasal polyp disease. J Allergy Clin Immunol.
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13. Nores JM, Avan P, Bonfils P. Medical management of nasal polyposis: a study in a
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14. Norlander T, Fukami M, Westrin KM, Stierna P, Carls B. Formation of mucosal

polyps in the nasal and maxillary sinus cavities by infection. Otolaryngol Head Neck
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15. Nucera E, Schiavino D, Milani A, Del Ninno M, Misuraca C, Buonomo A. Effects of

lysine-acetylsalicylate (LAS) treatment in nasal polyposis: two controlled long term
prospective follow up studies. Thorax. 2000 Oct. 55 Suppl 2:S75-8. [Medline].

16. Parnes SM. Targeting cysteinyl leukotrienes in patients with rhinitis, sinusitis and
paranasal polyps. Am J Respir Med. 2002. 1(6):403-8. [Medline].

17. Radenne F, Lamblin C, Vandezande LM, Tillie-Leblond I, Darras J, Tonnel AB.

Quality of life in nasal polyposis. J Allergy Clin Immunol. 1999 Jul. 104(1):79-84.

18. Rinia AB, Kostamo K, Ebbens FA, van Drunen CM, Fokkens WJ. Nasal polyposis: a
cellular-based approach to answering questions. Allergy. 2007 Apr. 62(4):348-58.

19. Saunders MW, Wheatley AH, George SJ, Lai T, Birchall MA. Do corticosteroids
induce apoptosis in nasal polyp inflammatory cells? In vivo and in vitro studies.
Laryngoscope. 1999 May. 109(5):785-90. [Medline].

20. Singh H, Ballow M. Role of cytokines in nasal polyposis. J Investig Allergol Clin
Immunol. 2003. 13(1):6-11. [Medline].
21. Steinke JW, Bradley D, Arango P, Crouse CD, Frierson H, Kountakis SE. Cysteinyl
leukotriene expression in chronic hyperplastic sinusitis-nasal polyposis: importance to
eosinophilia and asthma. J Allergy Clin Immunol. 2003 Feb. 111(2):342-9. [Medline].

22. Tuncer U, Soylu L, Aydogan B, Karakus F, Akcali C. The effectiveness of steroid

treatment in nasal polyposis. Auris Nasus Larynx. 2003 Aug. 30(3):263-8. [Medline].

23. Winestock DP, Bartlett PC, Sondheimer FK. Benign nasal polyps causing bone
destruction in the nasal cavity and paranasal sinuses. Laryngoscope. 1978 Apr.
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