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SHORT COMMUNICATION
Year : 2013  |  Volume : 4  |  Issue : 1  |  Page : 34-38

Spectrum of complications in sinusitis


Department of ENT, Father Muller Medical College, Mangalore, Karnataka, India

Date of Web Publication20-May-2013

Correspondence Address:
Mahesh Bhat
Department of ENT, Father Muller Medical College, Mangalore, Karnataka
India
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-9727.112278

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  Abstract 

Complications of paranasal sinus infection most often involve the orbit and peri-orbita. Because of widespread use of antibiotics, intracranial extension of paranasal sinusitis is rarely seen today. Nevertheless, the clinician must be aware of the potential of these complications as late recognition of this condition and delay in treatment can increase morbidity and mortality rates. An interesting case of sinusitis with orbital and intracranial complication is presented, which was radiologically evaluated and was comprehensively managed. Unparallel role of radiological investigations cannot be over emphasized as it played a very important role in both assessment and timing of the surgical intervention. The key to successful treatment is aggressive management and timely surgical intervention. We have extensively reviewed literature and comprehensively discussed pathophysiology and radiological assessment of such cases.

Keywords: Cavernous sinus thrombosis, intracranial suppurative complication, intraorbital complication, superior sagittal sinus thrombosis


How to cite this article:
Bhat M, Vaidyanathan V, Vishak S, Pinto G. Spectrum of complications in sinusitis. Muller J Med Sci Res 2013;4:34-8

How to cite this URL:
Bhat M, Vaidyanathan V, Vishak S, Pinto G. Spectrum of complications in sinusitis. Muller J Med Sci Res [serial online] 2013 [cited 2022 Jan 22];4:34-8. Available from: https://www.mjmsr.net/text.asp?2013/4/1/34/112278


  Introduction Top


Complications of paranasal sinus (PNS) infection most often involve the orbit and periorbita. Intracranial extension of sinus disease is infrequently seen today, the clinician may be unfamiliar with the evaluation and management of this potentially devastating complication. Despite recent advances in the treatment and diagnostic imaging, intracranial extension is often not recognized early enough to prevent delays in treatment aimed at reducing morbidity and mortality. [1],[2] Overlapping features of both acute sinusitis and early intracranial suppuration are seen in general, which clouded the initial diagnosis, even though the patient presented with eye involvement. Superior sagittal sinus thrombosis is relatively a rare dural venous sinus complication than cavernous sinus thrombosis (CVT) both of which were seen in our case. A kaleidoscopic neurological presentation and full recovery made by him at the time of discharge made this case more interesting. Intracranial complications are most often associated with infections of the frontal, ethmoidal, and sphnoidal sinuses. Maxillary sinusitis rarely extends intracranially; however, odontogenic maxillary sinusitis has shown an increased tendency for intracranial spread. [3] Complicated sinusitis can lead to brain abscess, subdural empyema, meningitis, CVT, epidural abscess and osteomyelitis, all occurring either alone or in various combinations.


  Case Report Top


A 20-year-old male patient presented to the Out Patient Department (ENT OPD), with c/o protrusion of the left eyeball, lid edema, headache, and spikes of high-grade fever with chills of 1 day duration. On further questioning, he had recurrent episodes of acute exacerbation of chronic sinusitis. On examination, he was lethargic but responsive and appeared toxic. He was febrile; his left eyeball was pushed outwards and downwards with lid edema and conjunctival congestion. Extra ocular movements were restricted in all directions but vision was normal. Diffuse swelling of left fronto - parietal region was present. Examination of nose revealed left alar and vestibular collapse, gross deviated nasal septum to left, mucopus in bilateral nasal cavities and all PNS were tender. There were no signs of meningeal irritation or any neurological deficits. Fundoscopic examination was normal. Preliminary blood investigations showed leucocytosis with neutrophil predominance. Computerized tomography (CT) scan of PNS showed pansinusitis with left orbital cellulitis with extra periosteal abscess with pneumocephalus [Figure 1]a and b. He was admitted and empirical treatment for acute sinusitis with inj. cefotaxime 1 g i.v. BD, inj. metronidazole 400 mg i.v. TID, inj. diclofenac sodium 50 mg i.m. BD and supportive measures was started. By day 2 in the hospital, the patient developed complete left external ophthalmoplegia with right lower limb grade 0/5 distal motor weakness. PNS were decompressed by endoscopic sinus surgery. Orbital abscess drained both internally and externally. On 3 rd post-operative day, he developed complete internal and external ophthalmoplegia of left eye with grade 0/5 proximal and distal right lower limb motor weakness with signs of meningeal irritation. Lumbar puncture was inconclusive. CT PNS and brain showed definite subdural empyema in relation to frontal lobe with cerebritis [Figure 2] indicating intracranial spread, which was not seen on the previous CT scan. Magnetic resonance imaging (MRI) and magnetic resonance venogram were suggested as the patient had neurological progression of the disease. To our astonishment, it showed partial thrombosis of superior sagittal sinus near the confluence and CVT [Figure 3], which in combination is a rare occurrence. Antibiotic (2 nd line) was changed to tazobactam-piperacillin 4.5 g i.v. TID, inj. amikacin 500 mg i.v. BD, anticonvulsants and diuretics were added. Neurosurgical intervention was sought and empyema was evacuated by burr hole of left frontal bone. Patient made full recovery over the next 1 month. He was regularly followed-up for 6 months and showed no signs of recurrence or neurological deficit.
Figure 1: (a) Computerized tomography scan image of case 1 on admission showing sinusitis with gross DNS to right with orbital abscess (air fluid level with hypodense opacity) displacing the eyeball downwards and outward. Intracranial air shadow seen in the left frontal region indicating pneumocephalus (up white arrow) and (b) orbital cellulitis with extra periosteal abscess displacing the eye ball anterior and laterally (white arrow)

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Figure 2: Computerized tomography scan image of case 1 on the 19th postoperative day showing a hypodense collection enveloped by a hyperdense shadow in form of a sac suggestive of an abscess

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Figure 3: Magnetic resonance venogram scan of case 1 showing filling defect in superior sagittal sinus (white arrow)

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  Discussion Top


Sinusitis is a relatively common problem encountered by an otorhinolaryngologist. Despite the advent of newer antibiotics, diagnostic procedures, and recent advances in management, it still precipitates with life threatening intracranial complications. [4]

The suppurative complications of sinusitis can be divided into intracranial and orbital. Orbital complications include pre-septal cellulitis, orbital cellulites with/without abscess and CVT. [5] Orbit is usually associated with disease involving the anterior ethmoidal air cells, characterized by peri-orbital edema, chemosis, visual loss, restriction of extra ocular movement (the lateral rectus is the earliest muscle to be involved with CVT causing diplopia as the abducent nerve supplying it is closely related) and proptosis. [6],[7] CVT typically presents with orbital apex syndrome (Proptosis, ophthalmoplegia, visual loss, V1 and V2 facial anesthesia) and venous thrombophlebitis causing episodes of high spiking fever. [8]

Orbital cellulitis and abscess are mainly diseases of children and adolescents, with a peak incidence during the first 15 years of age. In older ages, the disease is more severe and more pre-disposed to anaerobic infection. In case of orbital infection, clinical examination and prompt treatment are important, since any delay can result in serious complications, which include visual loss, intracranial and dural venous sinus spread. Visual loss is thought to be secondary to elevation of the intraorbital pressure caused by the accumulated pus, resulting in retinal ischemia due to central artery occlusion or thrombophlebitis along the valve less orbital veins. Visual loss may also occur because of optic neuritis due to extension of infection. Clinically, it difficult to differentiate between pre-septal cellulitis and abscess, in such conditions CT scan and MRI constitute important diagnostic aids. On the CT scan, the presence of abscess is suggested by a low density mass effect without enhancement, while the presence of air fluid level is a more specific finding of this condition. The medial displacement of medial rectus or the displacement of the periosteum away from the lamina papyracea constitute other characteristics of the abscess, while the swelling of the medial rectus muscle usually indicates orbital cellulitis. MRI is used mainly when intracranial spread is suspected. [9]

Intracranial complications include subdural empyema, epidural abscess, intracerebral abscess, meningitis, CVT, and other dural venous sinus thrombosis.

Prevalence of only 3.7% was reported by Claymen et al. in his retrospective study to assess the prevalence of intracranial complications of sinusitis (ICS) among all patients hospitalized for sinusitis. [10] The prevalence can vary from 3.7% to 47.6% according to various other studies however, sinus disease has been implicated as the underlying cause in about 10% of all causes of intracranial suppuration and 45% of these intracranial suppuration co-exist with orbital complication. [11]

Pathogenesis of ICS includes, two major mechanisms: Direct and indirect. Direct spread is by osteomyelitis and co-exists with underlying epidural abscess. Subdural empyema with epidural abscess would most commonly involve the frontal lobe secondary to direct spread from frontal sinus as a result of osteomyelitis of posterior table. If anterior table is involved, Pott's puffy tumor may occur. Indirect spread or commonly the retrograde thrombophlebitis is via the valve less diploe veins where there is no obvious bone erosion as we noticed in the above case. The infection can pass retrogradely into cavernous sinus and other dural venous sinuses. If the infection reaches the subdural spaces, it spreads easily over the convexities of brain owing to lack of septations. [12]

Most complicated sinusitis occurs in young men in the second or third decade of life as the frontal sinus continues to develop and the vascularity of diploeic veins is maximum in that period. In most of the studies, ICS are more commonly seen in males, with sex ratio ranging from 1.3:1 to 4.5:1. [10],[13] The most common presenting complaints are that of headache and fever. Nasal symptoms are prominent when gross-septal deviations or any other obstructive cause is present.

Suppuration from PNS would commonly cause meningitis but meningitis per se is not commonly due to sinus infection, as it is involved by hematogenous spread. Sphenoid and ethmoid air cell infection are commonly associated with meningitis. Headache and neck stiffness are universal complaints, patients appears toxic and febrile with nuchal rigidity, and often lumbar puncture clinches the diagnosis. Mental status at the time of diagnosis and the type of bacteria causing meningitis are the two most useful prognostic indicators in determining the final outcome. Overall fatality rate increases by 20% in adults if associated with meningitis. Sensorineural hearing loss and mild mental deficits are frequently observed late sequel. Gorse et al. [14] found an associated complication rate of 40% in patients undergoing treatment for meningitis, they include, sensorineural hearing loss, cranial nerve palsy, optic neuritis, and hemiparesis. Our patient did not have neurological deficit or meningitis on presentation or during post-operative period, probably that's why he had good prognosis.

Brain abscess in frontal and parietal lobes are often seen with frontal and ethmoid sinus infection. Chun et al. [15] in his study reported 40% of cases with brain abscess had permanent physical or mental disability, including hemiparesis, dysphagia, and blindness. Mental status and degree of orientation at the time of diagnosis are important prognostic indicators. Clinical features were non-specific, headache was the most common symptom, and early symptoms were due to increased intracranial pressure and often associated with seizures. Cerebritis is the initial stage in the development of brain abscess, which is intense focal intraparenchymal infiltration of inflammatory cells. If left untreated cerebritis will develop into frank abscess in 1 or 2 weeks-time. Timely CT with IV contrast detect this early cerebritis in selected patients. [16],[17] This can explain why in our case intracranial extension was not detected early.

Subdural empyema is the collection of frank pus between the dural and the arachnoid layer, most of the time it co-exists with epidural abscess. Of all intracranial suppurations, subdural empyema most commonly (41-67%) results from paranasal sinusitis (frontal) while other causes being meningitis, otitis media, operative injury, head trauma or bacteraemic seeding of a previous subdural hematoma. It is characteristically a rapidly progressive condition. Symptoms are reflective of increased intracranial pressure, meningeal irritation, and cerebritis. Meningism develops relatively easily and the most common symptoms are headache, fever, and neck stiffness. Focal neurological deficits unfold rapidly including, seizures, hemiparesis, aphasia, and coma. [4],[6] Kaufman et al. [13] in his study of 17 patients with subdural empyema found co-existing peri-orbital cellulitis in seven. Lumbar punctures in these cases were consistent with parameningeal infection.

In most cases, CT scan is often the first radiological investigation carried out in suspected cases of subdural empyema because of cost-factor, availability and visualization of the PNS and associated bony anatomy. Early changes of meningeal thickening and cerebritis might not be shown in CT until abscess develops therefore, MRI is preferred over CT as it is more sensitive in picking parenchyamal abnormalities [11] and this can delay the radiological confirmation of intracranial pathology. On CT scan the empyema appears as a thin, hypodense subdural lesion, with linear enhancement of the medial surface. The grey matter-white-matter interface is displaced inwardly. Mass effect is generally caused by edema and ischemia rather than mass effect from the abscess. The edema can cause effacement of the basilar cisterns and flattening of the cortical sulci. The sinuses might appear opacified, with air fluid levels and bony erosion evident in some cases. MRI appearance is similar; T1-weighted images show mass effect and hypointense areas of purulence, which are hyperintense on T2-weighted images. The abscess usually has a hyperintense rim on non-contrast T1-weighted images. Most empyemas are located within the frontal lobe. [18],[19]

Lumbar puncture is contraindicated in patients with subdural empyema if mass effect is present on CT or if patient has papilloedema as this can lead to tentorial herniation and even death. [13] Complications associated with subdural empyema are because of fatal dural venous thrombosis and coritcal infarctions, which appears to correlate with poor outcome. Mortality rate is up to 20% in such patients and 30% of those who survive will be neurologically impaired. [20] Subdural empyema is a true neurosurgical emergency, treatment includes, antimicrobial therapy against aerobic, anerobic cocci, and bacilli.

Third generation cephalosporins plus metronidazole offers broad coverage and good cerebrospinal fluid and abscess penetration. At least 2 weeks of intravenous therapy should be given, followed by oral therapy for up to 6-8 weeks. If adjacent osteomyelitis is present, prolonged intravenous therapy for a minimum period of 6-8 weeks should be considered. [10] Surgical management is an integral part and should not be delayed. The goals of surgical intervention are decompression of brain and complete evacuation of purulence. Vision impairment, as well as worsening of peri-orbital erythema or edema, proptosis and restriction of eye movements and lack of response to an initial trial of appropriate antibiotics is the absolute indications for surgical drainage. The route of surgical drainage is determined by localization of the orbital subperiosteal abscess, endoscopic orbital decompression or external approach can be employed. In addition, definitive management of intracranial suppuration should be done preferably at the same time. [9],[11]


  Conclusion Top


Intracranial and orbital complications are not as dreadful as they were earlier thought to be. The pathophysiology and clinical course has been well established and because of this understanding the disease can be mapped with CT and MRI and its' progression can be arrested with appropriate antibiotics and timely surgical intervention. Various prognostic indicators have been proposed to predict the outcome but we found absence of neurological deficits, good orientation, and absence of meningitis at presentation to be the most consistent and good prognostic indicators.

 
  References Top

1.Chalstrey S, Pfleiderer AG, Moffat DA. Persisting incidence and mortality of sinogenic cerebral abscess: A continuing reflection of late clinical diagnosis. J R Soc Med 1991;84:193-5.  Back to cited text no. 1
    
2.Wood MW, Cardenas R, Moore C. Influence of CAT scanning on diagnosis and mortality rate of brain abscess. J Tenn Med Assoc 1980;73:325-7.  Back to cited text no. 2
    
3.Courville CB, Rosenvold LK. Intracranial complications of infections of the nasal cavities and accessory sinuses. A survey of lesions observed in a series of fifteen thousand autopsies. Arch Otolaryngol 1938;27:692.  Back to cited text no. 3
    
4.Dolan RW, Chowdhury K. Diagnosis and treatment of intracranial complications of paranasal sinus infections. J Oral Maxillofac Surg 1995;53:1080-7.  Back to cited text no. 4
    
5.Goldberg AN, Oroszlan G, Anderson TD. Complications of frontal sinusitis and their management. Otolaryngol Clin North Am 2001;34:211-25.  Back to cited text no. 5
    
6.Jones NS, Walker JL, Bassi S, Jones T, Punt J. The intracranial complications of rhinosinusitis: Can they be prevented? Laryngoscope 2002;112:59-63.  Back to cited text no. 6
    
7.Singh B, Van Dellen J, Ramjettan S, Maharaj TJ. Sinogenic intracranial complications. J Laryngol Otol 1995;109:945-50.  Back to cited text no. 7
    
8.Giannoni CM, Stewart MG, Alford EL. Intracranial complications of sinusitis. Laryngoscope 1997;107:863-7.  Back to cited text no. 8
    
9.Vairaktaris E, Moschos MM, Vassiliou S, Baltatzis S, Kalimeras E, Avgoustidis D, et al. Orbital cellulitis, orbital subperiosteal and intraorbital abscess: Report of three cases and review of the literature. J Craniomaxillofac Surg 2009;37:132-6.  Back to cited text no. 9
    
10.Clayman GL, Adams GL, Paugh DR, Koopmann CF Jr. Intracranial complications of paranasal sinusitis: A combined institutional review. Laryngoscope 1991;101:234-9.  Back to cited text no. 10
    
11.Osborn MK, Steinberg JP. Subdural empyema and other suppurative complications of paranasal sinusitis. Lancet Infect Dis 2007;7:62-7.  Back to cited text no. 11
    
12.Wackym PA, Canalis RF, Feuerman T. Subdural empyema of otorhinological origin. J Laryngol Otol 1990;104:118-22.  Back to cited text no. 12
    
13.Kaufman DM, Miller MH, Steigbigel NH. Subdural empyema: Analysis of 17 recent cases and review of the literature. Medicine (Baltimore) 1975;54:485-98.  Back to cited text no. 13
    
14.Gorse GJ, Thrupp LD, Nudleman KL, Wyle FA, Hawkins B, Cesario TC. Bacterial meningitis in the elderly. Arch Intern Med 1984;144:1603-7.  Back to cited text no. 14
    
15.Chun CH, Johnson JD, Hofstetter M, Raff MJ. Brain abscess. A study of 45 consecutive cases. Medicine (Baltimore) 1986;65:415-31.  Back to cited text no. 15
    
16.Heineman HS. Bacterial brain abscess. Infectious Diseases and Medical Microbiology. 2 nd ed. Philadelphia: PA Saunders; 1986. p. 1080-5.  Back to cited text no. 16
    
17.Wenig BL, Goldstein MN, Abramson AL. Frontal sinusitis and its intracranial complications. Int J Pediatr Otorhinolaryngol 1983;5:285-302.  Back to cited text no. 17
    
18.Tsai YD, Chang WN, Shen CC, Lin YC, Lu CH, Liliang PC, et al. Intracranial suppuration: A clinical comparison of subdural empyemas and epidural abscesses. Surg Neurol 2003;59:191-6.  Back to cited text no. 18
    
19.Weisberg L. Subdural empyema. Clinical and computed tomographic correlations. Arch Neurol 1986;43:497-500.  Back to cited text no. 19
    
20.Haines SJ, Mampalam T, Rosenblum ML. Cranial and intracranial bacterial infections. In: Youmans JR, editor. Neurological Surgery: A Comprehensive Reference Guide to the Diagnosis and Management of Neurosurgical Problems. 3 rd ed., Vol. 6. Philadelphia: PA, Saunders; 1990. p. 3707-35.  Back to cited text no. 20
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]


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