1. Bailey Chase H. Miller Alfredo S.

Archilla
chapter 19 headache and facial pain
page 305
Headache and facial pain are a common complaint in
the otolaryngologist's office. Ninety percent of Americans
experience headache in their lifetime. Referral is often
made to determine if headache is sinus in origin, but in
this chapter we see that sinogenic causes of headache and
facial pain are infrequent. Primary headache disorders are
much more common. Secondary causes of headache and
facial pain comprise an extensive list. The otolaryngologist
should be able to identify sinus pathology and diagnose
and treat other common causes of headache.
Headache and facial pain can be grouped into primary.
secondary. and other etiologies. Primary headaches
include migraines, tension-type. cluster headaches, and
chronic daily headaches (CDHs). Other primary headache
disorders are beyond the scope of this chapter. Secondary
headaches include those that have specific etiologies identified.
This group can include trauma, vascular disorders,
infections, neuralgias, neoplastic causes, and others. Facial
pain can be divided into peripheral or central causes.
Peripheral facial pain makes up the larger of the two and
includes disorders of the head and neck that refer pain to
this region. Examples include temporomandibular joint
(TMJ) syndrome and various neuralgias. Central facial
pain is secondary to intracranial pathology like neoplasms
or vascular disorders. For simplicity, secondary headache
and peripheral facial pain disorders have been grouped
together in this chapter.
ANATOMY AND PHYSIOLOGY
The brain is not a sensory organ and therefore does not
perceive pain, but the surrounding structures in the brain
have nociceptive fibers that recognize pain. Intracranial
structures that are pain sensitive include major venous
sinuses, large cerebral vessels, upper cervical nerves, and
cranial nerves ( CNs) V. VII, IX. and X. The trigeminal nerve
and its branches provide the majority of the somatosensory
innervation to the head and face region. The trigeminal
nerve is a mixed nerve containing sensory and motor
components. The nerve exits the ventrolateral aspect of
the pons and divides into three main branches from the
Gasserian ganglion; the ophthalmic Vl, maxillary V2, and
mandibular V3 divisions. Disease in the anterior or middle
cranial fossa refers to the scalp or face anterior to the coronal
suture. Lesions of the posterior fossa structures refer to
the back of the head and upper neck. The sphenoid sinus
and sella refer to the vertex of the head. Pain from diffuse
intracranial disease may cause both anterior and posterior

head pain ( 1 ).
Electrical stimulation of the trigeminal ganglion causes a
cascade of events that are thought to cause headache. These
electrical impulses trigger neurogenic plasma extravasation.
This initiates a sterile inflammatory response, which leads
to pain. There is also an increase in extracerebral blood
flow and release of calcitonin gene-related peptide (CGRP)
and substance P (SP) (2). CGRP is the most potent peptide
vasodilator and its release causes vasodilation, mast cell
degranulation, and plasma extravasation. SP is involved in
inflammatory processes and pain perception. Pain impulses
from the dilation and inflammation are transmitted from
the trigeminal nerve to the trigeminal nucleus caudalis
('INC) in the brain stem. Because activation of the TNC can
result in referred migraine pain to the ophthalmic and maxillary
regions, patients may present with pain or pressure felt
around the eyes and sinuses. The superior salvatory nucleus
(SSN) that carries cranial parasympathetic fibers lies in close
proximity to the TNC. Stimulation of the TNC can cause
parasympathetic symptoms of rhinorrhea, congestion, and
lacrimation. A form of central sensitization takes place during
migraine. which is evident by symptoms of allodynia.
Allodynia is a common finding of pain from non-noxious
stimuli like touching the scalp or hair (Fig. 19.1 ).
305
306 Section 1: Basic Science/General Medicine
Vt- Ophthalmic n.
V2- Maxillary n. and
fOramen rotundum
V3- Mandibular n.
VII- Facial n.
N.C. - Nucleus Caudalis
L.G.- Lacrimal gland
SSN - Superior Salivatory
Nucleus
TG - Trigeminal ganglion
Figure 19.1 Trlgemlnal ne~rve~. V1, ophthalmic ne~rve;V2, maxll
lary nCINCI and forame~n rotundum; V3, mandibular nerve~; VII, fa
dal neNCI; NC, nudeus caudalls; LG, lacrimal gland; SSN, superior
sallvatory nudeus; TG, trigeminal ganglion; ION, Infraorbital ne~rve.
Depicted is the nigeminal nerve with ita three major
branches; ophthalmic, maxillary, and mandibular. The
1NC is close to the superior saliv.u:y nucleus (SSN), which
houses parasympathetic fibers. Activation of the TNC can
cause reflex activation of the SSN giving rise to rhinorrhea,
congestioJL and lacrimation.
PRIMARY HEADACHES
Migraine is the most common primar:y headache and one
of the leading causes of chronic illnesses and disability. Its
prevalence is estimated at 18% of the US female population

and 6% of the US male population (3). Two-thirds

of women experience migraine before or during menses
and these can worsen early in pregnancy. There ilJ a significant
decrease in episode frequency after menopause. About
70% of sufferers have a :first-degree relative with migraines.
Migraine headaches are recurrent attacks lasting 4 to
72 hours. They are usually unilateral, pulsatile in nature,
and of moderate to severe intensity. Attacks are often aggravated
by physical activity. They are associated with nausea
andfor photophobia and phonophobia. Most patients
report at least one nigger of their migraine headaches.
Common precipitating factoiS are emotional stress, hormonal
changes in women, fasting, weather changes, sleep
distwbances, odoiS, and alcohol ( 4 ).
Patients with migraine often have prodromal symptoms
such as neck stiffness, euphoria. depressiOIL fatigue,
anorma. food cravings, fluid retentiOJL drowsiness, and
enhanCEd alertness that begin 24 to 48 hours before the
onset of headache. Fifteen to thirty percent of migraine
sufferers have an aura preceding the pain. Auras are focal
neurologic symptoms presenting as visual, moto~ and sensory
distwbancea. Most auras develop slowly and may follow
one another in succession starting with visual symptoms
followed by sensoty distu!bances. VJ.Sual auras are most
common and often present as zigzag figures near the point
of fixation (fortification spectrum), moving geometric patterns,
flashes of light. and scotomas. Sensoty distwbances
are frequently described as pins and needles affecting a small
or l;uge area of one side of the body and face. Numbness
may also occur alone or in conjunction with other visual
and sensoty aurns. Some patients experience a postdromal
period where sudden head movements may precipitate short
luting pain in the location of the antecedent migraine headache.
During this period, some patients feel tired and othm
hiM! a sense of euphoria.
The diagnosis of migraine is clinical and relies on efficient
history taking skills and detailed physical exam. The
International Headache Society (IHS) divides migraines
into two major subtypes; migraine without aura and
migraine with aura. The latter is further subdivided into
(i) typical aura with migraine headache. (ii) typical aura
with nonmigraine headache, (iii) typical aura without
headache, (iv) familial hemiplegic migraine, (v) sporadic
hemiplegic migraine, (vi) basilar-type migraine. Each subtype
has speciftc diagnostic criteria (Thble 19.1). 1here are
no diagnostic testa for migraine and neuroimaging is not
necessary in most patienta. A head computed tomography
scan ( Cf) or magnetic resonance image (MRI) should be
obtained if there are unexplained abnormal findings on
neurologic examination, rapidly increasing frequency of

headaches and atypical headaches that do not fulfill the

strict diagnostic criteria established by the IHS.
Treatment for migraine headaches consists of acute headache
resolution, avoidanceofknown niggen, and prevention
of subsequent events. For mild to mode:rate nondisabling
pain, oral nonsteriodal anti-inflammatory drugs (NSAIDs ),
acetaminophen, and aspirin are appropriate first choice
agents. Caffeine may enhance the effect of the medications.
Some patients do not respond to mild analgesics and need
specific abortive the:rapies for acute migraine attacks. The
triptans are serotonin 1b/1d agonilJts that inhibit the release
of vasoactive peptides, promote vasoconstriction, and block
pain pathways in the brainstem. They are used in outpatient
situations because they are available in oral preparations,
nasal spl'a}'8. and subaltaneous injections (Thble 19.2).
Etgotamine and dihydroetgotamine are other abortive
therapies with similar pharmacology to the niptans,
which are commonly used in emergency rooms and hospitalized
patients. Ergots are serotonin 1b/d receptor and
alpha-adrenergic receptor blocke!s that cause arterial and
venous vasoconstriction. Dihydroergotamine is preferred
over ergotamine for its safety profile. It is available for
inttavenous, inttamusculat subcutaneous, and intranasal
use. .Antiemetics are also used, alone or in combination
with analgesics, for the treatment of acute migraine attacks.
Commonly used agenta include intravenous metoclopmmide,
intravenous and inttamuscular chlo~promazine.
SECONDARY CAUSES OF HEADACHE
Vascular: temporal arteritis, HTN, cavernous sinus thrombosis,
cerebral aneurysm, AV malformation
Musculoskeletal: neck and shoulder muscle contraction, strain
of extraocular or intraocular muscles, cervical spondylosis,
temporomandibular arthritis
Infections: meningitis, encephalitis, brain abscess, sepsis, sinusitis,
osteomyelitis, parotitis, mastoiditis, herpes zoster
Neoplasm: cerebral neoplasms, pheochromocytoma
Subdural hematoma
Cerebra I hemorrhage/infa ret
Pseudotumor cerebri
Normal pressure hydrocephalus
Post LP
Trauma
Dental: abscess, periodontitis, poorly fitting dentures
Neuralgia: sphenopalatine, glossopharyngeal, Sluder's, occipital
Eye: glaucoma
Metabolic: uremia, carbon monoxide inhalation, hypoxia,
hypoglycemia
Endocrine: hypothyroidism
Drugs: alcohol, nitrates, histamine antagonists
Paget disease of the skull
Effort induced: exertional, cough induced, coital cephalagia
Em otiona I/ psych iatric

migraine or probable migraine. Only 3% were diagnosed with

Ihinosinusitis (12). This can be confusing to the patient and
the clinician especially because it is not unusual for migraine
referred to the distribution of the trigeminal nerve to have
parasympathetic symptoms of Ihinorrhea. congestion, or lacrimation.

Those patients who do have headache and facial

pain from Ihinosinusitis often have associated symptoms of
nasal obstruction, hyposmia, or purulent nasal drainage. The
American Academy of Otolaryngology Head and Neck Swgery
includes headache as only a minor factor in the diagnosis of
acute Ihinosinusitis (Table 19.7). Facial pain alone does not
constitute Ihinosinusitis without another major factor.
HEADACHE ATTRIBUTED TO
RHINOSINUS (5)
Page 311 -312
Diagnostic criteria
A. Frontal headache accompanied by pain in one or more regions
of the face, ears, or teeth and fulfilling criteria C and D
B. Clinical, nasal endoscopic, CT and/or MRI imaging and/or
laboratory evidence of acute or acute-on-chronic rhinosinusitis
C. Headache and facial pain develop simultaneously with onset
or acute exacerbation of rhinosinusitis
D. Headache and/or facial pain resolves within 7 dafter
remission or successful treatment of acute or acute-on-chronic
rhinos inus it is

The IHS has specific criteria for headache due to rhinosinusitis.

Diagnosis requires a history of associated symptoms
and clinical evidence via examination or radiologic studies.
Nasal endoscopy, CI; or MRI can be used to determine the
presence of rhinosinusitis. The IHS classifies sinus headache
as a secondary diagnosis as illustrated in Table 19.8.
Headache from paranasal sinus disease is characterized
by deep, dull pain that may or may not pulsate. Typical
referral patterns exist as recorded in Table 19.9. Based on
the studies by Wolff most pain emanating from the sinuses
is related to inflammation and engorgement of the turbinates,
ostia, and nasal frontal ducts. Anatomical narrowing
can create contact points between mucosal surfaces. These
trigger points cause referred pain.
Other causes of headache include rhinitis, mucoceles,
neoplasm, and contact points. Nasal mucoceles or
neoplasms often reach a notable size before symptoms
of obstruction of the ostia cause pain and symptoms.
Nasal mucosal swelling and anatomical abnormalities
like concha bullosa or septal deflections can cause contact
points and theoretical pain. Release of SP can occur
locally and centrally through the trigeminal pathways.
Various studies have been performed to evaluate the
validity of contact points between membranes as the
cause of rhinogenic headache. Palpation of the contact
point or injection of Xylocaine with 1:100,000 epinephrine
to contact point during a headache has been tried.
Jones has, however, found that 50% of these contact
areas are on the side opposite the side of the pain (15).
Case reports and series exist showing improvement in
headache pain from 30% to 90% after surgical treatment
of these areas. Treatment varies from turbinate
reduction, septoplasty, to directed endoscopic ethmoidectomy.
Long-term studies by Welge-Luessen have been
performed with almost 10-year follow up revealing 65%
improvement (16). No controlled or randomized studies
have been performed to investigate the validity of
surgical treatment.

CRITERIA FOR DIAGNOSIS OF

RHINOSINUSITlS--2 MAJOR OR
1 MAJOR AND 2 MINOR (13)
Major FactDr
Facial pain/pressure
Facial congestion/fullness
Nasa I obstruction/hi ockage
Nasa I discharge/purulence/dis colored
postnasal drainage
Hyposmi a/anosmia
Purulence in the nasal cavity on exam
Fever (acute rhinosinusitis only)
Minor Factors
Headache

Fever (chronic)
Halitosis
Fatigue
Dental pain
Cough
Ear pressure/pain/
fullness

HEADACHE AND FACIAL PAIN

LOCATION IN ACUTE SINUSmS (14)

Paranasal Sinus Location of Pain

Frontal
Maxillary
Ethmoid
Sphenoid
Frontal region
Vertex
Over the antral area
Radiate to upper teeth
Forehead
Nasion
Retro-orbit
Radiate to temporal
Occipital
Vertex
Frontal region
Retro-orbit

Chapter 20 Complementary an Alternative Medicine

Li-Xing Man Nicholas C. Sorrel
Page 316-326
CAM FOR THE OTOLARYNGOLOGIST
Preyalence of CAM Use in Otolaryngology
Pat1ents
Patients with otolaryngologic complaints commonly use
complementary and alternative therapies. In a survey of
1, 789 patients presenting to an academic otolaryngology
practice in Scotland, 35% had used a CAM treatment in
the last 12 months and 18% had used the therapy for an
ear, nose, or throat condition ( 34, 35). Less than half of the
patients disclosed CAM use to their physicians. The same
group found similar responses in their rhinology and head
and neck oncology subspecialty clinics (36,37). A study
performed at an academic rhinology practice in Canada
found that 16% of patients diagnosed with chronic rhinosinusitis
had used a CAM therapy for their condition
(38). Another recent Canadian study of patients presenting
with thyroid nodules to a head and neck oncology
practice found that approximately one-half were on CAM
oral supplements and one-third of the patients reported
using supplements known to affect hemostasis (39). Other
investigators in the United States and Europe have found
lower prevalence of CAM use in head and neck oncology
patients ranging from 6 to 23% (40,41).
Practice Implications
Patients may not inform their physicians regarding CAM
use for a number of reasons. They may believe that products
are "natural and thus pose no potential for hann.
They may be concerned that the physician might impose
judgment for not using mainstream therapy, or they may
doubt the physician's knowledge and ability to provide
advice regarding CAM products. Although rare, the use of
CAM products has the potential-both theoretic and documentedto negatively impact prescribed medical and surgical
treatments. A recent survey of 844 patients presenting
to an outpatient clinic revealed that 15% were using herbal
medicines and 40% of these had potential herb-drug
interactions ( 42).
Drug-Herb Interactions
Although a complete list of potential herb-drug interactions
is beyond the scope of this chapter, some general
guidelines and common interactions are discussed. The
reader is referred to the resources listed in Table 20.1 to
research specific effects and interactions. In the United
States, the practitioner should report all suspected adverse
events to the United States Food and Drug Administration's
(FDA's) Medwatch Program (http:ffwww.fda.govfmedwatch)
and should encourage patients to inform use of supplements
to their pharmacists. When reviewing the literature
regarding herbal treatments, one must remember that the
evidence is largely anecdotal and based on case reports
(43). The preparation of supplements is not regulated by
the FDA There is heterogeneity in both potency and pu
Allergic Rhinitis and Rhinosinusitis

There are a myriad of CAM therapies for treating both allergic

rhinitis (103) and chronic rhinosinusitis. Few are studied
with rigorous double-blind RCTs for clinical efficacy.
Often, the pharmacologic mechanisms and adverse effects
are even less well understood. A few therapies for allergic
rhinitis, including spirulina, butterbur, and phototherapy
hold some promise.
Spirulina. the dried biomass of the blue-green algae
Arthospira platensis, is considered safe for consumption by
the FDA and is thought to inhibit histamine release from
mast cells (71, 104 ). RCTs have shown reductions in serum
IL-4 levels and clinical nasal symptom scores in allergic
rhinitis patients taking spirulina (105,106). Additional
studies are needed to determine the efficacy and the active
pharmacologic agent of spirulina.
The leaf and root extracts from the shrub butterbur
(Petasites hybridus) have been shown to inhibit leukotriene
and histamine synthesis ( 107) as well as mast cell
degranulation in vitro (108). Alkaloids that are hepatotoxic
and carcinogenic must be removed from raw butterbur
extract before it can be used (109). In RCTs, butterbur
was found to significantly improve nasal symptom scores
compared to placebo (110) and to be comparable in
efficacy to cetirizine (111) and fexofenadine (112,113).
Another RCT, however, found no difference in symptom
scores and peak nasal airflow compared to placebo (114).
Moreover, butterbur did not inhibit skin-test reactivity in
a study comparing butterbur to an antihistamine and placebo
using skin-prick tests (115). Although preliminary
data suggest butterbur may be effective in allergic rhinitis,
additional studies are needed to elucidate its efficacy and
safety.
Phototherapy with ultraviolet (UV) light is believed
to have immunosuppressive effects, including the reduction
of antigen presentation by dendritic cells, inhibition
of proinflammatory cytokine synthesis and release,
and induction of apoptosis in immune cells (116). A RCf
investigating the use of a combination of low-dose UV-B,
UV-A. and visible light in patients with ragweed-induced
allergic rhinitis resulted in decreased nasal symptom
scores and serum eosinophil levels ( 117). Phototherapy
was found to be superior to fexofenadine in the reduction
of rhinorrhea, nasal obstruction, and total nasal symptom
scores (118). However, it has not been directed compared
to intranasal corticosteroids. UV light induces DNA damage
and, at high doses, is associated with carcinogenesis.
The long-term effects of phototherapy on nasal mucosa
are unknown.
There are fewer studies on various CAM therapies for
rhinosinusitis compared to allergic rhinitis, and the existing
literature is more difficult to interpret because investigators
may use different definitions for acute and chronic
rhinosinusitis. Two of the best-studied CAM treatments
are sinupret and bromelain. Sinupret is an herbal preparation
containing extracts of elder flower, primrose flower,
common sorrel, vervain, and gentian root. Bioflavonoids
in sinupret have been found to stimulate transepithelial
chloride transport (119). For acute rhinosinusitis, one RCf
comparing sinupret to placebo as an adjunct to antibiotics
and a nasal decongestant showed significantly improved

radiographic and patient-assessed outcomes (120) while

another RCf found no difference between sinupret and
placebo (121).
Bromelain is the crude extract from the stem and immature
fruit of pineapple. It contains concentrates of closelyrelated
proteinases and is thought to prevent and reduce
edema. promote absorption of antibiotics, and induce production
of cytokines (122). A meta-analysis of two RCTs
found that bromelain decreased nasal mucosal inflammation,
nasal discomfort,. breathing difficulty, and overall
symptom scores compared to placebo ( 123 ). A number of
other herbal treatments have single studies showing positive
effects for rhinosinusitis, but these results have not
been replicated (123).
Honey made from the nectar obtained from manuka,
a small tree native to New Zealand, is believed to have
antibacterial and antifungal properties attributed to the
active ingredient methylglyoxal (124). Recently, manuka
honey has been shown to be effective against the biofilms
of Pseudomonas aeruginosa and Staphylococcus aureus,
including methicillin-resistantS. aureus (125). Treatment
of honey solution in an animal nasal mucosal model did
not show evidence of histologic epithelial injury (126).
In an RCf assessing the use of a sprayed manuka honey
solution in patients with allergic fungal rhinosinusitis,
patient-assessed symptom scores improved in those
treated with honey, but there were no differences in culture
results or endoscopy scores (127). The authors of this
chapter are currently conducting a RCf comparing topical
nasal irrigations with manuka honey solution to culturedirected
oral antibiotics for acute exacerbations of chronic
rhinosinusitis.
Tills chapter reviewed some of the main types of CAM utilized
by patients. Possible drug-herb interactions as well
as perioperative issues are discussed. Finally. the existing
evidence for CAM therapies used for ear, nose, and
throat diseases are reviewed. Given that a large number of
patients use CAM therapies, it is important that the practicing
otolaryngologist should have some insight into the
world of CAM.

MRI n CT Sinus : Chapter 27 page 422, 425,426, 449

 Acute Rhinosinusitis Chapter 33

Elizabeth K. Hoddeson Sarah K. Wise
Page 509-524 (543)
Sistemik Disease affect nose n sinus

RSK with nasal polyposis chapter 34

Patofisiologi Rinosinusitis
Zara M.. Patel Peter H. Hwang

Chapter 535
PATHOPHYSIOLOGY
Acute Rhinosinusitis
Etiologi dari rinosinusutis akut (RSA) lebih mudah ditemukan dibandingkan rinosinusitis kronik. Pada RSA
peran virus dan bakteri patogen telah ditentukan. RSA virus lebih umum dikenal dibandingkan RSA bakteri.
Pada orang dewasa, rata-rata pernah menderita dua sampai tiga kali infeksi virus pada saluran nafas atas setiap
tahunnya, banyak diantaranya melibatkan sinus paranasal. Angka kejadian secara spesifik tidak diketahui,
namun diperkirakan 39% sampai 87% dari infeksi virus akut saluran nafas atas menyebabkan rinosinusitis virus.
Rhinovirus merupakan penyebab dari hampir setengah kasus, dengan virus lainnya seperti coronavirus,
influenza, parainfluenza. respiratory syncytial virus, adenovirus,dan enterovirus merupakan sisanya. Seluruh
infeksi virus akut saluran nafas atas, hampir 0.5% sampai 2% akan mengalami komplikasi menjadi RSA
sekunder bakteri. Selama infeksi virus akut, mediator inflamasi multipel diregulasi. Inflamasi akut mukosa sinus
ditandai dengan hipersekresi mukosa dan edema, dapat menyebabkan obstruksi aliran sinus. Stasisnya mukus
menyebabkan lingkungan kaya akan proliferasi bakteri. Virus merusak dan meghancurkan epitel nasal dan
mengganggu klirens mukosilier. Selanjutnya membuat pasien cenderung mengalami infeksi sekunder bakteri.
Saat infeksi virus akut secara primer merupakan penyebab RSA bakteri, faktor host seperti infeksi gigi, penyakit
atofi, imunodefisiensi sistemik, disfungsi imunitas bawaan, atau obstruksi anatomi dapat merupakan faktor
predisposisi sekunder. Bakteri patogen penyebab RSA bakteri yaitu Streptococcus pneumoniae (33%),
Haemophilus influenzae ( 32% ), Staphylococcus aureus ( 10% ), dan Moraxella catarrhalis (9%). Sejak
dikenalkannya vaksin 7-valent pneumococcal untuk anak-anak, terdapat penurunan prevalensi S. Pneumoniae
dan meningkatkan H. infiuenzae pada dewasa dengan sinusitis maksila akut.

 SIGNS AND SYMPTOMS ASSOCIATED wnH DIAGNOSIS OF RHINOSINUS (1996

RHINOSINUS TASK FORCE) page 540
PREVENTION OF COMPLICATIONS OF SINUSITIS page 583-584

TREATMENT page 543-544

Acute Rhinosinusitis
Peresepan antibiotik The overprescribing of antibiotics is an issue affecting primary
care providers and otolaryngologists alike. High rates
of drug resistant infections have made the judicious, evidencebased use of antibiotics an imperative.
The first determinant in treatment of acute rhinosinusitis
is whether the infection is likely viral or bacterial.
Clinical guidelines have proposed that acute viral and bacterial
sinusitis generally cannot be differentiated until day
10 of symptoms, beyond which the infection is likely to be
bacterial ( 48). At day 10, antibiotic treatment is appropriate.
but reliable patients may also be observed, since the
rate of spontaneous improvement in ABRS is 40% to 60%.
Antibiotic treatment before day 10 of symptoms may be
appropriate in patients who have a relapse of symptoms
after initial improvement ("double worsening") or in
patients with severe symptoms.
Clinical trials for acute rhinosinusitis are difficult to
interpret because of highly variable diagnostic inclusion
544 Section II: Rhinology and Allergy
criteria. Systematic reviews suggest that antibiotics shorten
the duration of illness and may increase the rate of cure by
15% compared with placebo. Antibiotics may also decrease
the need for concomitant supportive medication (63-66).
If antibiotic therapy is chosen, the treatment regimen
should begin with a narrow spectrum antibiotic, broadening
coverage in the face of immunocompromise, failure to
respond to initial therapy, or specific culture results showing
resistance. The 2007 guidelines recommend amoxicillin as
an appropriate first line therapy. If patients fail to respond,
fluoroquinolones or high-dose amoxicillin-clavulanate
(4g/day) are recommended (1). Regional resistance rates
should be considered when prescribing. The duration of
therapy is generally recommended to be 10 days, although
this is based simply on the duration used in most clinical
trials, and has not been validated definitively (53).
As with trials examining antibiotics, studies of intranasal
steroid use in ABRS have used broad inclusion criteria,

and may not truly reflect the patient population defined

by our Task Force guidelines. However, a Cochrane review
in 2007 performed a meta-analysis of four double-blind
placebo-controlled trials and recommended use of intranasal
steroids in ABRS as monotherapy or as an adjunct to
antibiotics (67).
Buffered normal saline irrigation can be used via high
pressure or low pressure delivery systems to rinse the
nasal cavity. Decongestants and mucolytics can also be
used as supportive therapy, although care must be taken
in patients with high blood pressure when administering
oral decongestants, and patients must be counseled to
avoid prolonged use of topical nasal decongestants to avoid
developing rhinitis medicamentosa. Decongestants and
normal saline irrigation are both listed as optional under
the 2007 guidelines.
Complications of acute sinusitis are rare (estimated 1
in 1,000 cases of ABRS) but carry the potential for serious
morbidity and require urgent treatment. Severe headache,
altered mental status, high fever. and prostration should
alert the clinician to the possibility of intracranial extension
of infection. Meningitis, epidural abscess, cavernous
sinus thrombosis, or even frank brain abscess are potential
adverse sequelae. The presence of periorbital edema,
erythema, impaired extraocular motility, or diminished
visual acuity may indicate orbital extension of infection.
Prompt imaging with contrast is indicated to characterize
the presence and extent of extrasinus spread of infection,
and consideration must be given to urgent administration
of intravenous antibiotics and surgical treatment

Acute rhinosinusitis in children may also

cause retropharyngeal lymphadenitis. Suppuration of
these inflamed nodes can eventually culminate in abscess
formation. Early administration of antimicrobials in adult
patients has led to a decreased incidence of upper respiratory
tract infections and consequently significantly fewer
DNSis originating from this site. This trend has given way
to infections of odontogenic sources becoming the primary
source of deep neck infection in adults, recognizing a
strong association with poor oral hygiene and lower socioeconomic
status (2). Page 794
Currently, the oral antimicrobial classes
used to treat acute rhinosinusitis include b-lactams, fluoroquinolones,
macrolides/azalides, lincosamides, and
sulfonamides/trimethoprim with one ketolide as a possibility
(Table 97 .6). A complete discussion of these classes
of antibiotics is beyond the scope of this chapter but can
be found in the Supplement to Otolaryngology-Head and
Neck Surgery, Antimicrobial Treatment Guidelines for
Acute Bacterial Rhinosinusitis (29). Antibiotics should
be reserved for patients with bacterial. Page 1458

Di Ebook dr.puspa (E)

Dari THT MAMA RAJA ( THT KL D)

Dari THT MAMA RAJA ( THT KL D)

SAMPE (09022016):