Spontaneous Nasal Septal Abscess

J Med Sci 2005;25(5):251-254
http://jms.ndmctsgh.edu.tw/2505251.pdf
Copyright © 2005 JMS
Yuan-Heng Tsao, et al.
Spontaneous Nasal Septal Abscess
Yuan-Heng Tsao, Chao-Jung Lin, and Hsing-Won Wang*
Department of Otolaryngology-Head and Neck Surgery,
Tri-Service General Hospital, National Defense Medical Center,
Taipei, Taiwan, Republic of China
In the absence of early diagnosis and proper management, a nasal septal abscess, an uncommon entity, may lead to lethal
complications. It is most frequently seen in cases of traumatic septal hematoma with subsequent infection but also occurs in
cases of furunculosis of the nasal vestibule, sinusitis, influenza, and dental infection. To our knowledge, this is the first case
report of a nasal septal abscess developing spontaneously in an immunocompromised and coagulopathic patient. We report
this case to reinforce the need for scrupulous evaluation in immunocompromised and coagulopathic patients presenting with
nasal obstruction without a history of trauma.
Key words: nasal septum, spontaneous nasal septal abscess
INTRODUCTION
Nasal septal abscess (NSA) is defined as a collection of
pus between the cartilaginous or bony nasal septum and the
mucoperichondrium or mucoperiosteum1. NSA is uncommon and usually occurs subsequent to traumatic nasal
hematoma with infection. NSA is also less frequently
associated with nasal vestibular furunculosis, sinusitis,
influenza, and dental infection1-4. In cases presenting with
nasal obstruction but no history of preceding events such
as those mentioned above, the possibility of an NSA might
be ignored and the condition treated as for rhinitis with
septal deviation or thickened nasal septum5. The complications of an NSA, such as meningitis, brain abscess, subarachnoid empyema, and cavernous sinus thrombosis,
could be lethal. Other complications include saddle nose
deformity, septal perforation, and permanent nasal
obstruction1,2,6. Early diagnosis and proper management
are necessary to prevent the potentially dangerous spread
of infection and the development of severe functional and
cosmetic sequelae2.
We present an uncommon case of spontaneous NSA in
an immunocompromised patient with coagulopathy, to
Received: August 31, 2004; Revised: December 15, 2004;
Accepted: January 20, 2005.
*
Corresponding author: Hsing-Won Wang, Department of
Otolaryngology-Head and Neck Surgery, Tri-Service General Hospital, 325, Cheng-Gong Road Section 2, Taipei 114,
Taiwan, Republic of China. Tel: +886-2-8792-7192; Fax: +
886-2-8792-7193; E-mail: [email protected]
alert physicians to be more vigilant when this disease
presents. The etiology, pathogenesis, bacteriology, and
management of septal abscess are discussed.
CASE REPORT
A 63-year-old male presented to our emergency department with symptoms of frontal headache, nasal pain, and
nasal obstruction, which he had experienced for the previous month. He had received medical treatment at another
clinic for rhinitis with nasal septal deviation and thickened
nasal mucosa. He denied a prior history of nasal trauma,
sinusitis, epistaxis, or dental procedures, but had a history
of allergic rhinitis. The patient’s medical history included
type 2 diabetes mellitus, uremia with maintained hemodialysis, hepatitis B virus-related liver cirrhosis with
splenomegaly, anemia, thrombocytopenia, esophageal
varices, and hypertensive cardiovascular disease. On arrival,
the patient’s body temperature was 36.3oC without chills
and his blood pressure was 227/95 mm Hg. Physical
examination revealed erythematous skin of the nasal dorsum with saddle deformity. Bilateral dull purple swelling
of the nasal septum was noted. This swelling resulted in
total obliteration of the nasal airway (Fig. 1A). The nasal
septal swelling did not change in size when topical
oxymetazoline nasal spray was applied, and it fluctuated
when probed.
Other otolaryngological examinations were unremarkable. A complete blood cell count showed a raised
total white blood cell count of 11.10×103μ
/ L with a raised
differential count of 88.2% neutrophils, and a diminished
platelet count of 86×103/μL. The partial thromboplastin
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Spontaneous nasal septal abscess
Fig. 1 (A) Bilateral dull purple bulging of the nasal septum
resulting in total obliteration of the nasal airway. (B)
Axial computed tomography image with contrast showing swelling of the nasal septum with hypodense fluid
collection.
time and prothrombin time were within normal range.
However, bleeding time exceeded 15 minutes. A postcontrast axial and coronal computed tomography (CT) of
the paranasal sinuses showed a swollen anterior nasal
septum with central low-density fluid collection (Fig. 1B).
In view of the clinical symptoms and radiological
findings, the clinical impression was that of a nasal septal
abscess. Parenteral administration of antibiotic was initiated with 1.0 g intravenous cefazolin, which was followed
by 1.0 g intravenous cefazolin every 24 hours. The patient
underwent surgical drainage under general anesthesia after
the impaired hemostatic status had been corrected by
transfusion of 20 units of cryoprecipitate and intravenous
administration of desmopressin (16μg). A vertical 8 mm
incision was made through the dependent portion of the
right anterior nasal septum and 8 mL of pus was drained
from underside of the mucoperichondrium. The segmented
and necrotic septal cartilage was removed. The nose was
packed with Vaseline- and tetracycline-impregnated gauze,
and the incision wound was kept open with a wet dressing.
The patient’s headache subsided on the day following
the operation. We changed the wet dressing twice daily and
the nasal packing every 3 days. On day 6 of hospitalization,
conscious disturbance developed and infection with cranial spread was suspected. Cerebrospinal fluid analysis
252
Fig. 2 (A) Persistent saddle nose deformity. (B) Patency of the
patient’s nasal airway after treatment.
and magnetic resonance imaging of the brain were negative for intracranial infection. The antibiotic regimen was
changed to 1 dose of 1.0 g intravenous vancomycin and 1.0 g
ceftazidime every 12 hours for 3 days. Three days later, the
patient regained normal consciousness. The antibiotic regimen was then changed to 250 mg oral ciprofloxacin twice
daily because bacterial culture revealed the presence of
Pseudomonas aeruginosa, which is sensitive to ciprofloxacin. A follow-up examination 3 weeks after the operation showed that the septal abscess had subsided and the
wound had healed. The nasal airway was patent but saddle
nose deformity persisted (Figs. 2A,B).
DISCUSSION
An NSA is an uncommon entity. The incidence rate
does not appear to have been accurately documented. To
the best of our knowledge, major centers managed fewer
than 10 cases annually1,7. NSA most frequently results from
an infected nasal hematoma following nasal trauma1,8 and
is usually seen in younger patients1. Less frequently, NSA
is associated with a preceding event such as furunculosis of
the nasal vestibule, sinusitis, influenza, dental infection,
and nasal surgery1-4.
A spontaneous NSA is far less common than that associated with preceding events and may be missed as a
common cold or thickening of the mucoperichondrium, as
illustrated by our case. The uremic patient has bleeding
Yuan-Heng Tsao, et al.
diathesis, which aggravates the tendency for mucocutaneous bleeding because it affects serosal and mucosal
surfaces9. Ecchymoses and epistaxis are the major bleeding manifestations10. Thus, the etiology in our patient is
that the coagulopathy and immunocompromised status
predisposed him to spontaneous nasal septal hematoma
with subsequent opportunistic infection.
The most common presentation of the NSA is nasal
obstruction. Other signs and symptoms include nasal pain,
headache, fever, saddle nose, and swelling of the nasal
septum1. The nasal septum may be swollen and fluctuant
on palpation. Fine-needle aspiration together with CT
scanning with contrast enhancement may be helpful for
accurate diagnosis and identification of the area involved.
Physicians should be aware of the life-threatening complications of NSA, which include osteomyelitis, orbital
cellulitis, orbital abscess, intracranial abscess, meningitis,
and cavernous sinus thrombosis. Life-threatening complications in the immunocompromised patient may progress
rapidly if the NSA remains unchecked and untreated5. The
infection can spread via several routes. Orbital or periorbital complications are associated with the contiguous
invasion of the infection8. Further intracranial extension is
linked to the venous communication between the nasal
septum and facial angular and ophthalmic veins, which are
valveless and lead back to the cavernous sinus1. Moreover,
lymphatics of the superior meatus drain via the cribriform
plate and the vertical plate of the ethmoid bone into the
subarachnoid space. Perineural sheaths of the olfactory
nerve, transmitting through the cribriform plate, represent
avenues for intracranial invasion1. Additionally, functional and cosmetic sequelae may be secondary to ischemic
necrosis and bacterial destruction of the nasal septal cartilaginous or bony supports.
In general, adequate management of NSA consists of
prompt drainage and simultaneous intravenous administration of broad-spectrum antibiotics that can cross the
blood-brain barrier. Aggressive control and treatment of
underlying medical problems are also mandatory to prevent the infection from spreading rapidly. As illustrated in
this case, control of uremic bleeding diathesis is necessary
to prevent excessive intra-operative bleeding and accumulation of the hematoma. Control of blood sugar level is helpful in improving immune status.
A thorough understanding of the bacteriology of NSA is
helpful. The most common pathogen is Staphylococcus
aureus. Less frequently, Streptococcus pneumoniae, group
A beta hemolytic Streptococcus, anaerobes, Hemophilus
influenzae, and coliforms have been reported1. In this case,
the culture revealed Pseudomonas aeruginosa, which is an
opportunistic pathogen commonly seen in immunocompromised populations.
In conclusion, the possible existence of an NSA would
occur to physicians examining patients presenting with
nasal obstruction accompanied by preceding events. In our
case, there was no evidence of preceding trauma or other
sources of infection. In view of the patient’s underlying
medical problems, coagulopathy and immunocompromised
status predisposed the patient to progressive spontaneous
nasal hematoma and subsequent infection resulting in
abscess formation. We would like to emphasize that NSA
in patients with underlying impaired hemostatic and immune systems could develop silently. In cases of suspected
NSA, it is important that a thorough rhinologic examination is made and a detailed history obtained. In addition, it
is important to prevent disease progression by aggressive
treatment and control of underlying diseases.
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