spontaneus nasal septal abscess

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    Yuan-Heng Tsao, et al.J Med Sci 2005;25(5):251-254http://jms.ndmctsgh.edu.tw/2505251.pdfCopyright 2005 JMS

    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 Gen-

    eral 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]

    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 uncom-

    mon 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 suchas 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 complica-

    tions of an NSA, such as meningitis, brain abscess, sub-

    arachnoid 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 inan immunocompromised patient with coagulopathy, to

    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 depart-

    ment with symptoms of frontal headache, nasal pain, and

    nasal obstruction, which he had experienced for the previ-

    ous month. He had received medical treatment at anotherclinic 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 patients medical history included

    type 2 diabetes mellitus, uremia with maintained hemo-

    dialysis, hepatitis B virus-related liver cirrhosis with

    splenomegaly, anemia, thrombocytopenia, esophageal

    varices, and hypertensive cardiovascular disease. On arrival,

    the patients body temperature was 36.3oC without chills

    and his blood pressure was 227/95 mm Hg. Physical

    examination revealed erythematous skin of the nasal dor-

    sum with saddle deformity. Bilateral dull purple swellingof 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 unre-

    markable. A complete blood cell count showed a raised

    total white blood cell count of 11.10103/L with a raised

    differential count of 88.2% neutrophils, and a diminished

    platelet count of 86103/L. The partial thromboplastin

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    Spontaneous nasal septal abscess

    time and prothrombin time were within normal range.

    However, bleeding time exceeded 15 minutes. A post-

    contrast axial and coronal computed tomography (CT) ofthe 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 initi-

    ated 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 (16g). A vertical 8 mm

    incision was made through the dependent portion of theright 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 patients 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 cra-

    nial spread was suspected. Cerebrospinal fluid analysis

    and magnetic resonance imaging of the brain were nega-

    tive 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 regi-

    men was then changed to 250 mg oral ciprofloxacin twicedaily because bacterial culture revealed the presence of

    Pseudomonas aeruginosa, which is sensitive to cipro-

    floxacin. A follow-up examination 3 weeks after the opera-

    tion 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 fewerthan 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 asso-

    ciated 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

    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 show-

    ing swelling of the nasal septum with hypodense fluid

    collection.

    Fig. 2 (A) Persistent saddle nose deformity. (B) Patency of the

    patients nasal airway after treatment.

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    Yuan-Heng Tsao, et al.

    diathesis, which aggravates the tendency for mucocutane-

    ous bleeding because it affects serosal and mucosal

    surfaces9. Ecchymoses and epistaxis are the major bleed-

    ing 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 com-

    plications of NSA, which include osteomyelitis, orbitalcellulitis, orbital abscess, intracranial abscess, meningitis,

    and cavernous sinus thrombosis. Life-threatening compli-

    cations in the immunocompromised patient may progress

    rapidly if the NSA remains unchecked and untreated5. The

    infection can spread via several routes. Orbital or perior-

    bital 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 thesubarachnoid space. Perineural sheaths of the olfactory

    nerve, transmitting through the cribriform plate, represent

    avenues for intracranial invasion1. Additionally, func-

    tional and cosmetic sequelae may be secondary to ischemic

    necrosis and bacterial destruction of the nasal septal carti-

    laginous or bony supports.

    In general, adequate management of NSA consists of

    prompt drainage and simultaneous intravenous adminis-

    tration of broad-spectrum antibiotics that can cross the

    blood-brain barrier. Aggressive control and treatment of

    underlying medical problems are also mandatory to pre-

    vent the infection from spreading rapidly. As illustrated inthis case, control of uremic bleeding diathesis is necessary

    to prevent excessive intra-operative bleeding and accumu-

    lation of the hematoma. Control of blood sugar level is help-

    ful 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 revealedPseudomonas aeruginosa, which is an

    opportunistic pathogen commonly seen in immunocom-

    promised 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 patients 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 im-

    mune systems could develop silently. In cases of suspected

    NSA, it is important that a thorough rhinologic examina-

    tion is made and a detailed history obtained. In addition, it

    is important to prevent disease progression by aggressivetreatment and control of underlying diseases.

    REFERENCES

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    2. Matsuba HM, Thawley SE. Nasal septal abscess: un-

    usual causes, complications, treatment, and sequelae.

    Ann Plast Surg 1986;16:161-166.

    3. Pang KP, Sethi DS. Nasal septal abscess: an unusual

    complication of acute spheno-ethmoiditis. J LaryngolOtol 2002;116:543-545.

    4. da Silva M, Helman J, Eliachar I, Joachims HZ. Nasal

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    5. Shah SB, Murr AH, Lee KC. Nontraumatic nasal

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    6. Canty PA, Berkowitz RG. Hematoma and abscess of

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    7. Eavey RD, Malekzakeh M, Wright HT Jr. Bacterialmeningitis secondary to abscess of the nasal septum.

    Pediatrics 1977;60:102-104.

    8. Beck A. Abscess of the nasal septum complicating

    acute ethmoiditis. Arch Otolaryngol 1945;42:275-279.

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    esis and therapy. Am J Med Sci 1998;316:94-104.

    10. Remuzzi G, Schieppati A, Minetti L. Hematologic

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