overview surgical management of wegener's granulomatosis · overview surgical management of...

International Journal of Scientific & Engineering Research Volume 8, Issue 12, December-2017 1312 ISSN 2229-5518

IJSER © 2017 http://www.ijser.org

Overview surgical management of Wegener's granulomatosis.

Fahd Hamoud ali Altowairgi, Raad hameed altowairqi, Rayan Darwish Habib, Abdulaziz

Fahad Altowairqi, Rayan Mohammed Alofi

Abstract:

This review goes over the use of interventional surgeries to handle manifestations of Wegener's

granulomatosis triggered by tissue damage and scarring. These symptoms consist of nasal and

paranasal sinus illness, center ear inflammation, nasolacrimal duct obstruction, orbital

inflammatory masses, subglottic stenosis, tracheobronchial illness, and end-stage renal illness. A

search of literature through databases; MIDLINE, and EMBASE was conducted to

identified related articles to our concerned topic (management of Wegener's

granulomatosis) that were published up to November 2017. Wegener's granulomatosis

(WG) is a multisystemic illness advancing with granulomatous inflammation of the respiratory

system and characterized by necrotizing vasculitis and granuloma development, and its

tracheobronchial involvements result in stenosis. Otorhinolaryngologist is the very first physician

to contact for the majority of patients with GPA. Research studies, which showed up recently,

create prospect for the introduction of less harmful and more efficient therapy of GPA with

biological agents. In the advanced stages of WG, the infraglottic JV technique is a great choice

amongst techniques that can be utilized for enabling airway and for performing gas exchange

IJSER

http://www.ijser.org/



during surgical treatment conducted for granulations in the upper airway. In this method, the thin

framework of the catheter provides proper vision for surgical procedure and good working

conditions during resection with the CO2 laser and gives safe airway management and gas

exchange for anaesthetists.

Introduction:

Granulomatosis with polyangiitis (GPA) is a rare type of vasculitis. The term Wegener's

granulomatosis has largely been superseded by GPA which is taken into consideration to be a

more precise reflection of its aetiology [1] It is thought to be an autoimmune inflammatory

procedure affecting endothelial cells. It is a multisystem illness which can impact many parts of

the body, categorised by the ELK category: it most generally offers with lesions in the upper

respiratory system (E showing ears/nose/throat, nearly 100%), lungs (L most patients) and

kidneys (K > 75%). Numerous other locations of the body might additionally be affected, with

joint inflammation taking place in 25-50% of all instances. The sinuses, eyes and skin could

additionally be influenced [2], [3]

Subglottic stenosis found in 10-- 20% of WG patients can develop as the first searching for of the

illness or throughout the training course of the disease [5] In this case, the surgical target is to

eliminate the airway blockage by supplying an all-natural airway anatomy. While moderate

situations do not require surgical treatment, more serious set lesions need surgical interventions

such as tracheostomy, laser resection and dilatation [4].

IJSER




In patients that underwent tracheostomy, granulomas can happen in the tracheal tissue

surrounding the tracheostomy cannula. Endotracheal or tracheostomy tube cuffs lead to pressure

on respiratory tracts and mucosal trauma, and this excessive pressure triggers the formation of a

necrotic location as a circle, leading to eschar and stenosis [6] Moreover, the advancement of

inflammation and granulation tissue can form a severe stenosis in the airway. As a result, after

opening tracheostomy, decanulation of these patients can be difficult because of constant

development of the condition and restenosis. During the surgeries of these patients, airway

control is very important. If surgical treatment is for airway restoration, the scenario can be more

difficult and more complicated. In this instance record, gas exchange and airway management

supplied by jet ventilation (JV) during the excision of granulation tissue, which creates subglottic

stenosis in patients with WG, utilizing endolaryngeal laser surgery is discussed.

Wegener's granulomatosis (WG) is a rare systemic disease associated with necrotizing

granulomatous inflammation in the upper and lower respiratory tract, glomerulonephritis, and

vasculitis. This review goes over the use of interventional surgeries to handle manifestations of

Wegener's granulomatosis triggered by tissue damage and scarring. These symptoms consist of

nasal and paranasal sinus illness, center ear inflammation, nasolacrimal duct obstruction, orbital

inflammatory masses, subglottic stenosis, tracheobronchial illness, and end-stage renal illness.

Methodology:

A search of literature through databases; MIDLINE, and EMBASE was conducted to

identified related articles to our concerned topic (management of Wegener's

IJSER




granulomatosis) that were published up to November 2017, Following Mesh terms

were used in our search through the MIDLINE; “Wegener's granulomatosis”,

“management”. We limited our search to English language published articles with

human subject.

Discussion:

• Epidemiology

The occurrence of GPA is approximated to be 8- 10 cases per one million depending on

geographical location [7].It has been suggested that the incidence of GPA is increasing,

nevertheless this may just show the accessibility of new analysis techniques and serologic

examinations such as anti-neutrophil cytoplasmic antibodies (ANCAs) that enables a more

constant medical diagnosis [8].The age of signs beginning has a wide distribution with a peak

occurrence at 64- 75 years old [9].

Previous research studies showed that GPA can take place in kids with 8- 15% of cases taking

place in patients age 19 or more youthful [9].Although slight male predominance has been

reported in few instance series [10] a recent research consisting of 158 patients revealed no sex

preference [11].GPA is most frequently reported in white Caucasian patients yet can be seen in

all racial and ethnic groups [11].

IJSER




• Systemic manifestations

Classic GPA, as detailed by Godman and Churg in 1954 [12], includes the triad of necrotizing

granuloma of upper and lower breathing system, systemic vasculitis, and necrotizing

glomerulonephritis. The kidneys are generally spared in the restricted type of GPA. Classic GPA

can sometimes begin with minimal organ participation and after that transform to a much more

general type with nose, lung and kidney being influenced [14]. Patients with GPA generally

present with nonspecific symptoms of generalized systemic illness consisting of high

temperature, malaise, weight loss, arthralgia, and myalgia [13].

The earliest complaints, which are likewise the most common reasons for seeking medical

attention, are typically connected to upper respiratory tract problems including sinus pain,

purulent nasal discharge, epistaxis, nasal ulcer, and serous otitis media. The existence of clinical

signs such as suppurative otitis, mastoiditis, a saddle-nose defect, and hearing loss need to inform

the physician for GPA.It has been revealed that over 90% of patients with GPA have top

respiratory tract participation [11].A large number of patients present with pulmonary signs

(cough, hemoptysis, dyspnea and less frequently, pleuritic chest discomfort and tracheal

blockage). Reciprocal or independent pulmonary infiltrates exist in nearly 50% of patients

initially, with lung illness at some point establishing in 85- 90% of patients. Pleural effusion has

additionally been reported in 12% of instances [15].Grade Point Average can trigger significant

morbidity and death secondary to diffuse pulmonary hemorrhage [16].

Although kidney participation is clinically obvious in just 11- 20% of cases at presentation,

glomerulonephritis ultimately develops in 77- 85% of patients, usually within the initial two years

of condition beginning [13].Dermatologic involvement has been reported in concerning 50 % of

patients with GPA with purpura including the reduced extremities being one of the most typical

IJSER




searching for [11].Less typically, ulcers, blisters, papules, subcutaneous nodules and lesions

looking like those of pyoderma may be seen. Arthralgia and myalgia are seen in 70% of patients

[11].Nervous system participation is seen in regarding one-third of patients with outer

neuropathies being one of the most typical [17].Cranial neuropathies, exterior ophthalmoplegia,

seizures, cerebritis and stroke syndromes are additionally important findings. Diabetes insipidus

might take place when granulomas expand from the sinuses into the pituitary gland [17].Cardiac

participation is uncommon, with pericarditis being one of the most constant difficulties (6%).

Ocular manifestations

In a study of 701 North American patients with GPA, 30% of patients were reported to have

ocular participation [21].Other research studies have reported similar findings, with ocular

participation in regarding 50% of the patients [18].Ocular illness can be the presenting or even

the only clinically apparent indication of GPA [19].Straatsma classified the eye involvement as

adjoining or noncontiguous based on the existence or absence of direct extension from the

surrounding engaged sinuses [20].

Serious ocular morbidity with vision loss or overall blindness could be seen in 8- 37% of patients,

specifically if there has been a hold-up in medical diagnosis, or if the condition has been

improperly treated [18].

The Orbit

The orbit is one of the most regularly included ocular structure in GPA, and is more frequently

second to expansion of sinus pathology [19].Symptoms of orbital condition consist of proptosis,

lid edema, diplopia, and decreased vision. Orbital discomfort existed in only 30% of patients in

an Australian cohort. Of patients with orbital involvement, 14- 30% have bilateral illness.

IJSER




Damages to eye frameworks may result from mass compression, vascular occlusion or spread of

an orbital cellulitis. Proptosis happens in up to one-third of cases [11].GPA can offer as an orbital

mass bring about cranial nerve participation and entrapment of extraocular muscle resulting in

diplopia [22].Additionally, orbital participation could lead to blindness from a compressive

ischemic optic neuropathy [11].In a just recently published National Institutes of Health (NIH)

report, a group of 158 patients with GPA were examined and about half of patients with retro-

orbital participation lost vision [11].Orbital participation has additionally been reported in kids

[23].

The Lacrimal System

Inflammation of the lacrimal gland (dacryoadenitis) has been reported as an offering sign of GPA

[24].This presents with discomfort and edema of the anterior orbit in the superior-temporal region

with swelling of the eyelid and discomfort with eye motion. Nasolacrimal air duct obstruction is a

late searching for and is generally related to nasal involvement [25].Sicca disorder with positive

single strand A/ solitary strand B (SS-A/SS-B) auto-antibodies has additionally been reported.

The Episclera and Sclera

Both scleritis and episcleritis have been formerly reported in patients with GPA. GPA can result

in nodular, diffuse, or necrotizing scleritis with tendency towards a much more severe scleritis

compared with various other etiologies. Necrotizing scleritis could lead to considerable ocular

morbidity with serious vision loss and blindness if not adequately dealt with. Difficulties consist

of globe perforation needing enucleation [26].In necrotizing scleritis, an area of the inflamed

sclera comes to be avascular and ischemic, usually second to occlusive vasculitis. Hoffman et al.

[30] reported scleritis to be the 3rd most usual ocular symptom of GPA adhering to orbital and

IJSER




nasolacrimal involvement. Necrotizing scleritis has been reported complying with regular cataract

surgical treatment in patients with GPA. In some patients, it has been the here and now indication

of GPA, while in others, it occurred in spite of being in remission [27].

The Cornea

PUK is one of the most considerable corneal complication of GPA. On histopathology, there is an

immune-mediated occlusive necrotizing vasculitis of the anterior ciliary arteries. These arteries

supply the anterior segment of the eye consisting of the sclera, conjunctiva and the outer cornea.

Concentration of this hematologic inflammatory milieu in the peripheral cornea results in

ulceration of the peripheral corneal proteoglycans and collagen. This can advance concentrically

and/or centrally and is usually reciprocal. Owing to the shared blood supply, PUK is often

accompanied by scleritis (generally necrotizing) [28] It has been proposed that necrotizing

scleritis with PUK might define systemic vasculitis [29].While PUK is the prototypical corneal

complication in GPA, numerous various other corneal indications have likewise been described.

Sometimes, the nearby scleral inflammation results in an exudative peripheral keratitis without

ulceration. Stromal (interstitial) keratitis, is a hardly ever defined feature of GPA.

The Uvea

Although uncommon in isolation, intraocular inflammation has been described in patients with

GPA. The uveitis connected with GPA is nonspecific, unilateral or bilateral and can be anterior,

intermediate, or back with or without vitritis [19].An evaluation of a large cohort of patients with

anti-neutrophil cytoplasmic antibodies (ANCA) favorable vasculitis found an incidence of 17.9%

for uveitis: 70% anterior uveitis, 10% intermediate uveitis, and 20% posterior uveitis. The writers

noted that 50% of patients with anterior uveitis had an existing together scleritis (sclera-uveitis),

IJSER




recommending that usually uveitis was a secondary sensation [31].Additionally a granulomatous

panuveitis has been referred to as the preliminary symptom of GPA [32].

Table 1. Profile of Organ Involvement in Wegener Granulomatosis [19],[31][28].

Organ Site Frequency at Presentation, % Frequency During Disease Course, %

Upper airway 73 92

Lower airway 48 85

Kidney 20 80

Joint 32 67

Eye 15 52

Skin 13 46

Nerve 1 20

• Surgical care

Surgical treatment may be needed for:

o Nasal deformity. o Subglottic stenosis. o Obstruction of lacrimal ducts. o Bronchial stenoses. o Eustachian dysfunction (insertion of grommets). o Acute kidney injury (renal transplant). • Lacrimal drainage surgery in Wegener's granulomatosis

Nasolacrimal air duct blockage in Wegener's granulomatosis most likely takes place as a straight

extension of nasopharyngeal disease and typically is a late manifestation. Postoperative wound

necrosis and the development of nasocutaneous fistula have been reported after DCR in these

patients [33] and dacryocystectomy has been suggested as a therapy for nasolacrimal duct

IJSER




obstruction in this disease [34].Others have additionally reported much more motivating results

with DCR [35] or have recommended using endoscopic DCR in Wegener's disease [36].

In today series, all the patients offered in the third to 6th years, and either had a short (4- 5 years)

or lengthy (8- 30 years) history of symptoms suitable with Wegener's granuloma. Four patients

(patients 1, 2, 7, and 10) underwent uneventful and effective DCR on their regular maintenance

dose of immunosuppressants and three (patients 6, 8, and 11) achieved symptomatic relief with

perioperative immunosuppression. Patient 3 attained a good outcome with a short course of high

dose prednisolone following discovery of inflamed tissue at the personnel website. In patient 4,

the granulomatous illness had been quiescent for over 10 years, but the comprehensive scarring in

the nose was related to thick membrane layer formation over the rhinostomy and failure; surgical

treatment on the contralateral side, without adjuvant systemic immunosuppression, was curative.

Despite prednisolone and azathioprine cover, there was an intraorbital development of the nasal

granuloma through the rhinostomy in one patient (patient 5), this orbital condition settling with

boosted immunosuppression and later on surgery to the various other eye was straightforward

after giving prophylactic high dosage systemic steroids. Wegener's condition was not

acknowledged in patient 9 and numerous previous attempts of endoscopic laser DCR (before

reference) were without immunosuppression and associated with substantial nasal scarring and

development of a massive intranasal cyst-- these modifications undoubtedly compromising the

definitive lacrimal surgery. Endoscopic DCR may be inappropriate in the visibility of significant

nasal inflammatory illness, as illustrated in this situation, and we take into consideration that the

huge rhinostomy achievable with external surgical treatment could aid in the long term success of

the operation. There have been comparable recommendations for patients with sarcoidosis who

are undergoing lacrimal surgery [37]. On the other hand with a previous record [33] injury death

IJSER




and nasocutaneous fistula were not seen in our collection and there was just one very early failure

as a result of canalicular occlusion developing in a thoroughly marked nasal space.Open DCR

recommend as a safe and effective therapy for nasolacrimal blockage in patients with controlled

Wegener's granulomatosis. A rise in systemic immunosuppression ought to be considered for a

few weeks after surgical procedure in unstable condition, or when energetic illness is seen during

surgical procedure, and the patient monitored carefully for recurring or spreading postoperative

disease.

• Airway Surgery in Tracheostomised Patients with Wegener Granulomatosis Leading

to Subglottic Stenosis

Subglottic stenosis accompanying the proliferative development of diseased tissue in the direction

of the larynx and trachea in WG can cause airway blockage and require intervention. This

scenario is extra common in the 4th and 5th decades of life, and its symptoms vary from

coughing and lack of breath to serious stridor that is progressively dangerous. Around 16-- 23%

of these patients create subglottic stenosis, and this generally advances with fibrosis and oedema

causing stenosis that is 3- 4 centimeters below the singing cord. In a collection consisting of 7

patients, which was carried out by Alaani et al. [38], in the case of active illness, tracheostomy

was suggested as the initial surgical therapy selection in addition to clinical therapy for dealing

with respiratory system failure. In both our patients, surgical tracheostomy was carried out due to

the advancement of serious respiratory system distress and stridor associated with the progression

of the disease while clinical therapy was being gotten.

The development of the disease continues in patients with tracheostomy, and the formation of

granulomas bordering the tracheostomy cannula and extending downwards creates major stenosis

in the airway.

IJSER




As necessary, a new medical treatment is needed within the procedure. Lebovics et al. [39]

reported the presence of subglottic stenosis in 25 of 158 patients with WG, and they specified that

the lesion was so significant that some treatments such as dilatation, laser resection or

laryngotracheoplasty would be needed in 16 of these patients. In both our patients, subacute

degeneration on the basis of chronic condition and serious inspiration trouble despite

tracheostomy established, and a brand-new evaluation was demanded. First of all, the exact areas

and levels of sores were identified with the help of pictures obtained via CT, and

tracheobronchoscopy was executed under basic anaesthesia for the intervention plan of therapy.

Throughout basic anaesthesia applied in tracheobronchoscopy, which is performed for the

assessment of the lesion and for preparing surgical treatment and then used in the treatment for

the airway, airway control is necessary. Gao et al. [40] observed tracheal stenosis and dyspnoea

in 12 of 15 patients having a mass in the trachea. In these patients, basic orotracheal intubation

was favored for stenoses, triggering narrowing less than 50% in the throat lumen, and the

tracheostomy was opened in the mass situated in the upper area of the trachea. On the other hand,

in patients with a mass located in the lower area of the trachea and with significant respiratory

distress and hypercarbia, adequate oxygenation can not be provided with the conventional

method. For airway control in these patients, extracorporeal circulation wased initially used, and

passing an endotracheal tube with a stenotic lesion with a fibre-optic bronchoscope was after that

carried out as an alternative method. As another technique, Xu et al. [41] reported that an

adequate surgical site and suitable surgical atmosphere were supplied without any development

of any difficulty by protecting spontaneous respiration under infusion with propofol and

remifentanil without endotracheal intubation in 31 patients that were to undertake upper airway

surgical treatment.

IJSER




In the 10-year empirical study, Jaquet et al. [42] brought the subglottic JV onward as a choice to

the options of intubation with a little endotracheal tube, tubeless ventilation with the defense of

spontaneous respiration, and apneic oxygenation in the pathologies causing stenosis in the larynx.

The JV method can be assessed as a choice for the resection of granulation tissue with a CO2

laser owing to its thin catheter framework and feature of laser resistance. In our patients, the JV

strategy was used for the resection of granulation tissue, which surrounded the existing

tracheostomy, with a CO2 laser.

Conclusion:

Wegener's granulomatosis (WG) is a multisystemic illness advancing with granulomatous

inflammation of the respiratory system and characterized by necrotizing vasculitis and granuloma

development, and its tracheobronchial involvements result in stenosis. Otorhinolaryngologist is

the very first physician to contact for the majority of patients with GPA. This medical diagnosis

must constantly be taken into consideration in patients with recurring upper respiratory system

infections, otitis, mucosal ulcers and laryngitis. Proper and early diagnosis is crucial for imminent

treatment application and allows avoiding irreparable organ damage. Research studies, which

showed up recently, create prospect for the introduction of less harmful and more efficient

therapy of GPA with biological agents. In the advanced stages of WG, the infraglottic JV

technique is a great choice amongst techniques that can be utilized for enabling airway and for

performing gas exchange during surgical treatment conducted for granulations in the upper

airway. In this method, the thin framework of the catheter provides proper vision for surgical

procedure and good working conditions during resection with the CO2 laser and gives safe

airway management and gas exchange for anaesthetists.

IJSER




Reference: 1. Jennette JC; Nomenclature and classification of vasculitis: lessons learned from

granulomatosis with polyangiitis (Wegener's granulomatosis). Clin Exp Immunol. 2011 May164 Suppl 1:7-10. doi:

2. Pai S, Panda M; Limited Wegener's granulomatosis presenting as lung nodules in a patient with rheumatoid arthritis: a case report. Cases J. 2008 Dec 231(1):417. doi: 10.1186/1757-1626-1-417.

3. Holle JU, Moosig F, Dalhoff K, et al; Conditions in subjects with rheumatic diseases: pulmonary manifestations of vasculitides. Arthritis Res Ther. 2011 Jun 3013(3):224. doi: 10.1186/ar3307.

4. Yazıcı ZM, Kayhan FT, Erdur Ö, Erol BS. Granülomatoziste KBB tutulumu. KBB ve BBC Dergisi. 2009;17:62–5.

5. Zycinska K, Wardyn K, Zielonka TM, Nitsch-Osuch A, Zarzycki S, Demkow U, et al. Subglottic and tracheal stenosis due to Wegener’s granulomatosis. Adv Exp Med Biol. 2013;755:221–4.

6. Grillo HC, Donahue DM, Mathisen DC, Wain JC, Wright CD. Postintubation tracheal stenosis. J Thorac Cardiovasc Surg. 1995;109:486–92.

7. Ntatsaki E, Watts RA, Scott DG. Epidemiology of ANCA-associated vasculitis. Rheum Dis Clin North Am. 2010; 36:447-461.

8. Andrews M, Edmunds M, Campbell A, Walls J, Feehally J. Systemic vasculitis in the 1980s ?is there an increasing incidence of Wegener's granulomatosis and microscopic polyarteritis? J R Coll Physicians Lond. 1990; 24:284-288.

9. Hoffman GS, Kerr GS, Leavitt RY, Hallahan CW, Lebovics RS, Travis WD, Rottem M, Fauci AS.Wegener granulomatosis: An analysis of 158 patients. Ann Intern Med. 1992; 116:488-498.

10. Walton EW. Giant-cell granuloma of the respiratory tract (Wegener's granulomatosis). Br Med J. 1958; 2:265-270.

11. Hoffman GS, Kerr GS, Leavitt RY, Hallahan CW, Lebovics RS, Travis WD, Rottem M, Fauci AS.Wegener's granulomatosis: An analysis of 158 patients. Ann Intern Med. 1992; 116:488-498.

12. Godman CC, Churg J. Wegener's granulomatosis: Pathology and review of the literature. AMA Arch Pathol. 1954; 58:533-553.

13. Fauci AS, Haynes BF, Katz P, Wolff SM. Wegener's granulomatosis: Prospective clinical and therapeutic experience with 85 patients for 21 years. Ann Intern Med. 1983; 98:76-85.

14. Specks U, DeRemee RA. Granulomatous vasculitis. Wegener's granulomatosis and Churg-Strauss syndrome. Rheum Dis Clin North Am. 1990; 16:377-397.

15. Cordier JF, Valeyre D, Guillevin L, Loire R, Brechot JM. Pulmonary Wegener's granulomatosis. A clinical and imaging study of 77 cases. Chest. 1990; 97:906-912.

IJSER




16. Leavitt RY, Fauci AS, Bloch DA, et al. The American College of Rheumatology 1990 criteria for the classification of Wegener's granulomatosis. Arthritis Rheum. 1990; 33:1101-1107.

17. Nishino H, Rubino FA, DeRemee RA, Swanson JW, Parisi JE. Neurological involvement in Wegener's granulomatosis: An analysis of 324 consecutive patients at the Mayo Clinic. Ann Neurol. 1993; 33:4-9.

18. Spalton DJ, Graham EM, Page NG, Sanders MD. Ocular changes in limited forms of Wegener's granulomatosis. Br J Ophthalmol. 1981; 65: 553-563.

19. Cogan D. Corneoscleral lesions in periarteritis nodosa and Wegener's granulomatosis. Trans Am Ophthalmol Soc. 1955; 53: 321-342.

20. Straatsma BR. Ocular manifestations of Wegener's granulomatosis. Am J Ophthalmol. 1957; 144:789-799

21. Abdou NI, Kullman GJ, Hoffman GS, Sharp GC, Specks U, McDonald T, Garrity J, Goeken JA, Allen NB. Wegener's granulomatosis: Survey of 701 patients in North America. Changes in outcome in the 1990s. TJ Rheumatol. 2002; 29:309-316.

22. Cassan SM, Divertie MB, Hollenhorst RW, Harrison EG., Jr Pseudotumor of the orbit and limited Wegener's granulomatosis. Ann Intern Med. 1970; 72:687-693.

23. 30. Ziakas NG, Boboridis K, Gratsonidis A, Hatzistilianou M, Katriou D, Georgiadis NS. Wegener's granulomatosis of the orbit in a 5-year-old child. Eye. 2004; 18:658-660.]

24. Howe L, D'Cruz D, Chopdar A, Hughes G. Anterior ischaemic optic neuropathy in Wegener's granulomatosis. Eur J Ophthalmol. 1995; 5:277-279.

25. Kalina PH, Garrity JA, Herman DC, DeRemee RA, Specks U. Role of testing for anticytoplasmic autoantibodies in the differential diagnosis of scleritis and orbital pseudotumor. Mayo Clin Proc. 1990; 65:1110-1117.

26. Foster CS, Forstot SL, Wilson LA. Mortality rate in rheumatoid arthritis patients developing necrotizing scleritis or peripheral ulcerative keratitis. Effects of systemic immunosuppression. Ophthalmology. 1984; 91:1253-1263.

27. Sainz de la Maza M, Foster CS. Necrotizing scleritis after ocular surgery. A clinicopathologic study. Ophthalmology. 1991; 98:1720-1726.

28. Messmer EM, Foster CS. Vasculitic peripheral ulcerative keratitis. Survey of ophthalmology. 1999; 43:379-396.

29. Watson PG, Mason S. Fluorescein angiography in the differential diagnosis of sclerokeratitis. Br J Ophthalmol. 1987; 71:145-151.

30. Hoffman GS, Kerr GS, Leavitt RY, Hallahan CW, Lebovics RS, Travis WD, Rottem M, Fauci AS.Wegener granulomatosis: An analysis of 158 patients. Ann Intern Med. 1992; 116:488-498.

31. Watkins AS, Kempen JH, Choi D, Liesegang TL, Pujari SS, Newcomb C, Nussenblatt RB, Rosenbaum JT, Thorne JE, Foster CS, Jabs DA, Levy-Clarke GA, Suhler EB, Smith JR. Ocular disease in patients with ANCA-positive vasculitis. J Ocul Biol Dis Infor. 2009; 3:12-19.

IJSER




32. Huong du LT, Tran TH, Piette JC. Granulomatous uveitis revealing Wegener's granulomatosis. J Rheumatol. 2006; 33:1209-1210.

33. Jordan DR, Miller D, Anderson RL(1987) Wound necrosis following dacryocystorhinostomy in patients with Wegener's granulomatosis. Ophthalmic Surg 18:800–803.

34. Holds JB, Anderson RL, Wolin MJ(1989) Dacryocystectomy for the treatment of dacryocystitis in patients with Wegener's granulomatosis. Ophthalmic Surg 20:443–444.

35. Hargwig PW, Bartley GB, Garrity JA(1992) Surgical management of nasolacrimal duct obstruction in patients with Wegener's granulomatosis. Ophthalmology 99:133–139.

36. Wong RJ, Gliklich RE, Rubin PA, et al.(1998) Bilateral nasolacrimal duct obstruction managed with endoscopic techniques. Arch Otolaryngol Head Neck Surg 124:703–706.

37. Chapman KL, Bartley GB, Garrity JA, et al.(1999) Lacrimal bypass surgery in patients with sarcoidosis. Am J Ophthalmol 127:443–446.

38. Alaani A, Hogg RP, Drake Lee AB. Wegener’s granulomatosis and subglottic stenosis: management of the airway. J Laryngol Otol. 2004;118:786–90.

39. Lebovics RS, Hoffman GS, Leavitt RY. The management of subglottic stenosis in patients with Wegener’s granulomatosis. Laryngoscope. 1992;102:1341–5.

40. Gao H, Yi J, Huang YG. Airway management and anesthesia for tracheal masses in 15 patients. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2013;35:322–6.

41. Xu J, Yao Z, Li S, Chen L. A non-tracheal intubation (tubeless) anesthetic technique with spontaneous respiration for upper airway surgery. Clin Invest Med. 2013;36:151–7.

42. Jaquet Y. Complications of different ventilation strategies in endoscopic laryngeal surgery. Anesthesiology. 2006;104:52–9. IJSER


overview surgical management of wegener's granulomatosis · overview surgical management of...

Documents