Conservative Management of Necrotizing Fasciitis of the Eyelids Jason A. Luksich, MD,1 John B. Holds, MD,1,2 Morris E. Hartstein, MD1 Objective: To describe the management of patients with necrotizing fasciitis of the eyelids. Design: Retrospective, noncomparative interventional case series. Participants: Seven patients with necrotizing fasciitis limited to the eyelids. Methods: Retrospective review of the charts and photographs of seven patients with necrotizing fasciitis limited to the eyelids. Main Outcome Measures: Eyelid function and appearance, mortality, and morbidity. Results: Seven of seven patients had good eyelid function and adequate appearance without reconstruction after healing. No deaths occurred. Conclusions: Eyelid necrosis due to necrotizing fasciitis can be a devastating condition. The morbidity and mortality of selected cases are reduced with prompt and appropriate antimicrobial therapy and nonaggressive debridement of necrotic tissue after autodemarcation of the necrotic zone. Ophthalmology 2002;109:2118 –2122 © 2002 by the American Academy of Ophthalmology, Inc.
Necrotizing fasciitis is the anatomical description that Wilson1 first used to describe the extensive necrosis of the subcutaneous tissues that is most frequently caused by a rapidly spreading infection of Streptococcus pyogenes in the subcutaneous plane. There are numerous case reports in the medical literature describing these devastating infections, which involve limbs, the abdominal wall, and the perineum.2– 6 Aggressive surgical debridement has been described as essential to proper management of these infections. Although necrotizing fasciitis of the head and neck is rare, it can involve the skin and subcutaneous tissues of the eyelid. Involvement of the eyelid is often preceded by regional minor soft tissue trauma and is frequently associated with diabetes and alcohol abuse.3 Necrotizing fasciitis of the eyelids has been reported after blepharoplasty.7,8 On the basis of a literature review, Kronish and McLeish4 reported the mortality of patients with periorbital spread as 12.5%. They found the prognosis to be affected by delay in diagnosis and treatment, by extension of infection from the face to the neck, or by both of these. Early debridement has also been advocated as crucial in the successful treatment of necrotizing fasciitis.2– 6,9,10 We believe that because of the rich local vascular supply and thin eyelid skin, necrotizing fasciitis limited to the eyelids may be treated differently. Patients may be treated with intravenous antibiotics and Originally received: November 12, 2001. Accepted: April 25, 2002. Manuscript no. 210573. 1 Saint Louis University Eye Institute, Department of Ophthalmology, Saint Louis University School of Medicine, St. Louis, Missouri. 2 Department of Otolaryngology, Head and Neck Surgery, Saint Louis University School of Medicine, St. Louis, Missouri.
delayed bedside debridement after autodemarcation of the necrotic margins. In some cases, surgical debridement may not be necessary at all.
Patients and Methods Medical charts and photographs of seven patients with necrotizing fasciitis limited to the eyelids were reviewed. Relevant details of presentation and management are discussed. A summary of patient characteristics is listed in Table 1.
Case Reports Case 1 A 59-year-old female awoke with swelling of her right eyelids without a history of trauma. She gave a history of a sinus infection 2 days previously. On examination, her eyelids were edematous, with purulent drainage (Fig 1A). The patient was begun on intravenous ceftriaxone, gentamicin eye drops, and bacitracin ointment to the eyelids. Blood cultures were positive for group A streptococcus susceptible to the antibiotic regimen. Over the next 3 days, necrotic crusts formed on her upper eyelid in the area noted to be blanched at presentation (Fig 1B). The eyelid margins and adjacent skin were spared. Bacitracin irrigation with wet to dry dressings to the lids was used to remove and debride necrotic tissue. No surgical debridement was performed. The eyelid margins and adjacent skin were spared. The patient completed a 10-day course of intravenous ceftriaxone as an outpatient. Without any further treatment, the patient continued to heal uneventfully, with satisfactory eyelid function (Fig 1C).
Case 2 Reprint requests to Morris E. Hartstein, MD, Saint Louis University Eye Institute, 1755 South Grand Boulevard, St. Louis, MO 63104. E-mail:
[email protected].
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© 2002 by the American Academy of Ophthalmology, Inc. Published by Elsevier Science Inc.
A 42-year-old male with a history of alcohol abuse and deep venous thrombosis presented with abrasion of the left upper eyelid ISSN 0161-6420/02/$–see front matter PII S0161-6420(02)01257-5
Luksich et al 䡠 Necrotizing Fasciitis of the Eyelids
Figure 1. A, Case 1 at presentation, demonstrating edema, expression of pus, and demarcation of infection. B, Case 1 at day 4, demonstrating necrosis of the upper and lower right eyelid with sparing of eyelid margins. C, Case 1 at 4 months after initial presentation, showing resolution of infection without surgical debridement of necrotic tissue.
1 day after a fall. Over the day preceding presentation, he noted rapidly progressive swelling of the eyelids on the left with increasing pain. On presentation, he was noted to have tense fluctuant swelling of the upper and lower eyelid on the left, with a purplish discoloration of the preseptal upper and lower eyelid skin and an advancing margin of erythema consistent with periorbital erysipelas (Fig 2A). Blood cultures were drawn, and the patient was
started on intravenous nafcillin, penicillin, and gentamicin. He was taken to the operating room, where he underwent drainage of abscesses from the upper and lower eyelids with cultures. In the hospital, he rapidly demarcated the areas of necrotic tissue comprising the majority of the purplish preseptal skin noted at presentation. The eyelid margins and adjacent skin were spared. After debridement (removal of necrotic tissues with forceps and
Figure 2. A, Case 2 at presentation, with a purplish necrotic area (small arrows) autodemarcating, showing the advancing edge of erythema (large arrows). B, Case 2 at 14 days after demarcation and debridement of necrotic tissue.
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Ophthalmology Volume 109, Number 11, November 2002 Table 1. Patient Patient No.
Age (yrs)/Sex
Type and Site of Injury
Area of Infection
Medical History
Wound Culture Results
1
59/F
No antecedent trauma
RUL, RLL
Group A Streptococcus
2
42/M
Blunt trauma, abrasion eyelids left
LUL, LLL
Alcoholic, h/o DVT
4⫹ Group A Beta-hemolytic Streptococcus
3
41/M
Injury right periorbital area 5 days PTA
RUL, RLL
Depression, anxiety
4
48/M
Squeezed carbuncle on nasal bridge
RLL
5
46/M
Fall with forehead abrasion 2d. PTA
RUL, RLL, LUL, LLL
IDDM, renal failure, arteritis on prednisone Alcoholic
Group A Streptococus Staphylococcus aureus Enterobacter sp. All cultures negative
6
36/M
Human bite RLL
RLL
7
49/M
Minor trauma eyelid
LUL, LLL, mild Rt side
Smoking alcohol abuse
Heavy Streptoccus pyogenes, light Staphylococcus aureus Mixed aerobe/anaerobe infection Group A Streptococcus
RUL ⫽ Right upper lid; RLL ⫽ Right lower lid; LUL ⫽ Left upper lid; LLL ⫽ Left lower lid.
scissors) without anesthesia, wet to dry dressings and warm soaks were applied. Initial blood and wound cultures grew a heavy growth of S. pyogenes, with a light growth of Staphylococcus aureus from the abscess cultures. On day 3, the patient was changed to intravenous clindamycin, and on day 6, he was discharged on a 14-day course of this. He continued to heal uneventfully, with adequate eyelid function and no need for reconstruction (Fig 2B).
Results The results of our study are summarized in Table 1. Seven patients were identified: one (14%) female and six (86%) males, who ranged in age from 36 to 59 years (mean, 45.8 years). Trauma was the cause of infection in six (86%) of the seven cases. Alcohol abuse was a contributing factor in three cases. One of the patients had diabetes and was receiving steroid treatment. The infection was unilateral in five of seven cases and bilateral in the other two cases. Group A -hemolytic streptococcus was the most common isolate. S. aureus, Enterobacter, and unidentified anaerobes were also grown out of wound cultures. Patient 4 had negative cultures, possibly from prior antibiotic treatment. However, clinically the patient clearly had necrotizing fasciitis. It should also be noted that this group of patients was treated in different facilities over 17 years, thus accounting for different antibiotic regimens. The broadspectrum approach reflects the concern for occult organisms or mixed infections. Surgical debridement occurred in five of seven cases. No debridement was performed in two of the cases. Bedside debridement occurred in only three of the cases, whereas two of the cases had initial debridement completed in the operating room. Five of seven patients had good lid function without surgery after completion of healing. An adequate outcome was poor appearance with good function, whereas an excellent outcome was good appearance with good function. Follow-up ranged from 1 to 24 months, with an average follow-up of 7.8 months. Two patients were lost to follow-up after the 1-month visit while still granulating defects, but they maintained good eyelid function at this visit, and no reconstructive surgery was anticipated for these patients.
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Discussion Necrotizing fasciitis can be a devastating condition. Even in the era of modern antibiotic therapy, mortality rates as high as 89% have been reported.5 Involvement of the extremities, trunk, and pelvis is the most common and carries the highest risk of mortality. The head and neck are only rarely involved. Necrotizing fasciitis involving the lower face and neck has a reported death rate of 32%,4 generally thought to be due to the spread to cervical and thoracic regions. Necrotizing fasciitis involving the scalp and upper face has a better prognosis, with 12.5% mortality reported by Kronish and McLeish.4 No deaths have been reported that are directly attributable to necrotizing fasciitis limited to the eyelids, although morbidity is significant.3 Sepsis also seems to be less common with necrotizing fasciitis of the eyelids, in contrast to necrotizing fasciitis of other areas.3 We hypothesize that necrotizing fasciitis involving the eyelids behaves differently than that involving other body sites because of the unique anatomic features of the eyelids. Differences in behavior include a lower incidence of sepsis, characteristic limited anatomic distribution at presentation, frequent arrest of progression with appropriate antibiotic therapy, apparent lower mortality, and autodemarcation of necrotic tissue, with the ability to debride conservatively in cases that arrest with antibiotic therapy. The eyelids tend to be resistant to infection because of their rich vascular supply.6 This rich vascular supply may allow for delayed debridement,11 because systemic antibiotics have better access to infected areas and the marginal zone of tissue adjacent to necrotic tissue maintains a better local blood supply.12 An interesting feature of the cases presented is the preservation of the eyelid margin and adjacent pretarsal skin and subcutaneous tissues after autodemarcation (Fig 2B). Rarely, surgeons may encounter pa-
Luksich et al 䡠 Necrotizing Fasciitis of the Eyelids Characteristics Days Before Therapy
Parental Antibiotics
0
Ceftriaxone
1
Nafcillin, penicillin, tobramycin
5 1 1 1 2
Debridement
Abscess Formation
Outcome
No surgical debridement Drainage in OR HD#1, subsequently bedside
None
Cipro, clinda, vanc, fluconazole
Necrotic tissue removed HD#4
None
Adequate appearance and function without surgery
Initial oral cephalexin, then oxacillin, ceftriaxone Nafcillin, penicillin, gentamicin, clindamycin
Necrotic tissue removed HD#9
Yes, drained ⫻2
Adequate appearance and function without surgery
Drainage, bedside debridement
Yes
Adequate lid function with significant soft tissue defect
Penicillin, tobramicin, clindamycin Penicillin, nafcillin, tobramycin
Minimal bedside debridement None
Yes
Excellent appearance and lid function without surgery Excellent appearance and lid function without surgery
tients with necrotizing fasciitis involving full-thickness eyelid or orbital tissues. These cases fall outside of our experience here. The low incidence of necrotizing fasciitis involving the head and neck might be attributed to the excellent blood supply to these tissues, although some early cases may go unrecognized because they resolve, albeit slowly, during treatment with high-dose broad-spectrum antibiotics.13 Necrotizing fasciitis is characterized as extensive necrosis of the superficial fascia, with widespread extension into surrounding tissues and secondary gangrene of the overlying skin.14 However, the skin of the eyelids is thin; that of the medial upper eyelid is the thinnest found in the body.15 The thin eyelid skin and lack of subcutaneous fat between the skin and orbicularis muscle allows necrotizing fasciitis involving the eyelids to run a different course than elsewhere on the body. Necrosis of the thin eyelid skin occurs rapidly, so the eyelids are a site that is unlikely to harbor a smoldering nidus of infection. Infection is less likely to extensively spread while it is hidden from view, as it can in other body sites. The external prominence of the eyelids may also prompt patients to present early in the infection. The orbicularis muscles deep to the subcutaneous layer may sometimes act as a barrier to the spread of periorbital necrotizing fasciitis. Laterally and inferiorly, the dermis is more firmly attached at the nasojugal and malar furrows. These lines may act as anatomic barriers because of the associated firm attachments to the dermis, which limits the spread of inflammation from the orbit.3 In addition, the dermis becomes much thicker over the malar folds and eyebrows. The path of least resistance for the subcutaneous spread of edema and inflammation is over the nasal bridge to the contralateral lids. This may explain the high incidence of bilateral necrotizing fasciitis.3 Edema of the loose subcutaneous eyelid tissues is typically well demarcated, with a specific border at the surrounding areas having a denser subcutaneous fibroadipose.14 Inoculation by trauma to the
Yes
None
Adequate appearance and function without surgery Adequate lid function with soft tissue defect
Comment
⫹ blood cultures for Streptococcus pyogenes on presentation
Deceased 2 years later due to complication renal failure
forehead or parietoccipital region resulting in necrotizing fasciitis of the eyelids is not clearly understood (case 2). Most likely, it is due to venous seeding of the eyelids because of the rich anastomosis between the eyelids and the forehead and temporal region.3 Debate may occur over nomenclature in the definition of any disease process. The terms necrotizing fasciitis, erysipelas with eyelid necrosis, and streptococcal eyelid necrosis have all been applied to the clinical syndrome described herein.2– 6,11–13 Additionally, Shindo et al.,16 in a review of necrotizing fasciitis of the face, noted the synonymous terms necrotizing erysipelas, gangrene, necrotizing cellulitis, and necrotizing myositis as being inaccurately applied to necrotizing fasciitis. They suggested a strict definition of necrotizing fasciitis to include extensive necrosis of the superficial fascia, rapid spread to involve the surrounding tissue, and systemic toxicity. Not all of our cases would qualify as necrotizing fasciitis under this strict definition, because they did not demonstrate systemic toxicity. Nonetheless, the cases presented and reviewed by prior authors are clinically and phenomenologically similar to previously reported cases of necrotizing fasciitis of the eyelids. Because this was a retrospective case series with two independent clinicians’ (JBH and MEH) cases, the treatment protocol evolved in an ad hoc fashion. Retrospectively, we recommend inclusion criteria for allowing medical therapy and autodemarcation of patients with necrotizing fasciitis of the eyelids. We recommend this protocol for necrotizing fasciitis localized to the periorbital area with minimal systemic toxicity, with rapid demarcation of the edge of erythema and zone of necrotic tissue, and with no suggestion of orbital extension. Case 3 presented with septic shock. He was closely observed and responded well to our treatment protocol, although an argument could have been made in this case for more aggressive surgical therapy. Our treatment protocol differs from that of prior authors:
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Ophthalmology Volume 109, Number 11, November 2002 we recommend initial wound and blood cultures and appropriate antibiotic therapy covering Streptococcus pyogenes and other organisms that may be involved in the pathogenesis of necrotizing fasciitis of the eyelids.17 Initially, broad coverage for Streptococcus species, clostridia, and mixed organisms, using piperacillin/tazobactam, for example, is warranted. Once a species is identified, antibiotics can be adjusted accordingly. If S. pyogenes is isolated, ceftriaxone (possibly with clindamycin) is very effective. Consultation with the infectious disease service may be helpful. If a subcutaneous abscess is present, we recommend draining it to decompress the overlying soft tissue and decrease the infectious load. Obviously, necrotic tissue may be debrided at this time. The patient is then observed, because a clear zone of demarcation will appear over the next few days, allowing further debridement, generally at the bedside. Bedside debridement refers to removal of the necrotic tissues with forceps and scissors, usually without anesthesia. This can be done in an operating room, but it can often be accomplished at the bedside after autodemarcation. It is the authors’ experience that the line demarcating the edge of the infection does not advance after the institution of antibiotic therapy and that the area of necrotic eyelid tissue seen with autodemarcation is significantly less than the amount of tissue one would debride if aggressively debriding to the edge of the advancing infection, as described by other authors.2– 6 Patients with uncomplicated periorbital necrotizing fasciitis can be treated conservatively with good results. Prospective or case-control studies and additional case reports would help to further support the authors’ concepts. It should be noted that even though we are advocating conservative management, all patients with suspected necrotizing fasciitis of the eyelids should be monitored extremely closely. Conservative management should never allow one to relax observation in this potentially very aggressive and destructive entity.
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2. Bisno AL, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med 1996;334:240 –5. 3. Overholt EM, Flint PW, Overholt EL, Murakami CS. Necrotizing fasciitis of the eyelids. Otolaryngol Head Neck Surg 1992;106:339 – 44. 4. Kronish JW, McLeish WM. Eyelid necrosis and periorbital necrotizing fasciitis. Report of a case and review of the literature. Ophthalmology 1991;98:92– 8. 5. Urschel JD, Takita H, Antkowiak JG. Necrotizing soft tissue infections of the chest wall. Ann Thorac Surg 1997;64:276 – 9. 6. Placik OJ, Pensler JM, Kim JJ, et al. Necrotizing periorbital cellulitis. Ann Plast Surg 1993;31:369 –71. 7. Suner IJ, Meldrum ML, Johnson TE, Tse DT. Necrotizing fasciitis after cosmetic blepharoplasty. Am J Ophthalmol 1999;128:367– 8. 8. Ray AM, Bressler K, Davis RE, et al. Cervicofacial necrotizing fasciitis. A devastating complication of blepharoplasty. Arch Otolaryngol Head Neck Surg 1997;123:633– 6. 9. Knudtson KJ, Gigantelli JW. Necrotizing fasciitis of the eyelids and orbit. Arch Ophthalmol 1998;116:1548 –9. 10. Shayegani A, MacFarlane D, Kazim M, Grossman ME. Streptococcal gangrene of the eyelids and orbit. Am J Ophthalmol 1995;120:784 –92. 11. Marshall DH, Jordan DR, Gilberg SM, et al. Periocular necrotizing fasciitis. A review of five cases. Ophthalmology 1997;104:1857– 62. 12. Scott PM, Bloome MA. Lid necrosis secondary to streptococcal periorbital cellulitis. Ann Ophthalmol 1981;13:461–5. 13. Rose GE, Howard DJ, Watts MR. Periorbital necrotising fasciitis. Eye 1991;5:736 – 40. 14. Jordan DR, Mawn L, Marshall DH. Necrotizing fasciitis caused by group A streptococcus infection after laser blepharoplasty. Am J Ophthalmol 1998;125:265– 6. 15. Lemke BN, Lucarelli MJ. Anatomy of the ocular adnexa, orbit, and related facial structures. In: Nesi FA, Lisman RD, Levine MR, eds. Smith’s Ophthalmic Plastic and Reconstructive Surgery, 2nd ed. St. Louis: Mosby, 1998; 3–78. 16. Shindo ML, Nalbone VP, Dougherty WR. Necrotizing fasciitis of the face. Laryngoscope 1997;107:1071–9. 17. Elliott D, Kufera JA, Myers RAM. The microbiology of necrotizing soft tissue infections. Am J Surg 2000;179:361– 6.