Ophthal Plast Reconstr Surg, Vol. 31, No. 2, 2015
Orbital Necrotizing Fasciitis and Osteomyelitis Caused by Arcanobacterium Haemolyticum: A Case Report Lindsay A. Stone, M.D., M.Sc.*, and Raymond J. Harshbarger III, M.D., F.A.C.S., F.A.A.P.† Abstract: The facial region is infrequently affected by necrotizing infections. Orbital necrotizing infections are even rarer, seen following trauma, local skin infection, and sinusitis. The authors report a unique case of orbital necrotizing fasciitis and osteomyelitis resulting from Arcanobacterium Haemolyticum ethmoid sinusitis. No prior occurrences of Arcanobacterial species orbital necrotizing fasciitis/osteomyelitis have been reported. A 16-year-old boy presented to the ER with a 3-day history of fever, chills, headache, and sinus pressure. CT scan revealed soft tissue swelling of the right orbit, forehead, and ethmoid sinusitis. Within 24 hours of admission, he suffered rapidly progressive swelling and erythema of the right orbit and forehead with diminished visual acuity, despite broad-spectrum antibiotics. Orbital exploration revealed frankly necrotic fascia and periosteum along the superior aspect. Lateral canthotomy, cantholysis, decompression of the optic nerve, and soft tissue debridement with bone biopsy was performed. Operative specimens isolated Arcanobacterium Haemolyticum. Pathologic examination revealed right orbital osteomyelitis.
N
ecrotizing fasciitis is a deep soft tissue infection with a predilection for the fascial layers. Tissue destruction is rapidly progressive and therefore requires timely diagnosis and treatment. Treatment of necrotizing fasciitis of any etiology necessitates aggressive tissue debridement and initiation of broad-spectrum antibiotics. Arcanobacterium haemolyticum has been implicated as a causal agent in infections including orbital cellulitis and sinusitis,1,2 necrotizing fasciitis of the extremity,3 osteomyelitis, wound infection, and abscess. Arcanobacterium haemolyticum can also be found as normal human flora and is often isolated in combination with other pathogens. Though most commonly implicated as a cause of pharyngitis4 in the pediatric population, the incidence is still rare. Diagnosis and treatment of Arcanobacterium haemolyticum infections can be challenging due to their relative infrequency. Furthermore, many laboratories do not routinely culture for Arcanobacterium haemolyticum, thus contributing to unrecognized infections or delays in diagnosis. However, there is no consensus regarding the optimal antibiotic treatment regimen for Arcanobacterium haemolyticum infections. The authors present a case of orbital necrotizing fasciitis with osteomyelitis caused by Arcanobacterium haemolyticum in an otherwise healthy adolescent male. Necrotizing fasciitis of the face is relatively uncommon, and a case of orbital necrotizing fasciitis with osteomyelitis secondary to Arcanobacterium haemolyticum has not been reported to the best of our knowledge. This case study was conducted in full compliance with
Accepted for publication August 30, 2013. *Oregon Health & Science University, Portland; †Craniofacial & Pediatric Plastic Surgery, Dell Children’s Medical Center of Central Texas, University Medical Center at Brackenridge, Austin, Texas, U.S.A. The authors have no financial or conflict of interest to disclose. Address correspondence and reprint requests to Raymond J. Harshbarger, III, M.D., F.A.C.S., F.A.A.P., Craniofacial & Pediatric Plastic Surgery, Dell Children’s Medical Center of Central Texas, University Medical Center at Brackenridge, Austin, TX 78723. E-mail: [email protected] DOI: 10.1097/IOP.0000000000000057
Case Reports
Health Insurance Portability and Accountability Act guidelines, and patient consent for the use of photography was obtained. Objective. To draw attention to a rare but significant pathogen as the etiologic factor in orbital necrotizing fasciitis.
CASE DESCRIPTION A 16-year-old man without significant medical history presented to the ER with a 4-day history of OD pain, swelling, nasal congestion, chills, headache, and sinus pain. He denied any recent trauma to the eye. The patient denied regular use of medication, had no known drug allergies, and was up to date on immunizations. He had presented to an outside ER the previous day, but after a negative workup for Strep throat and influenza, he was given prochlorperazine and discharged home. Physical examination revealed a drowsy but arousable adolescent man with right-sided periorbital swelling and erythema, proptosis, and decreased extraocular movements on the right (Fig. 1). Laboratory investigations on admission showed a white blood cell count of 19.9 × 103 cells/μL, 64% neutrophils, and bandemia with 26% band cells. A CT of the orbit demonstrated swelling in the right frontal and periorbital regions with air densities adjacent to the right frontal sinus (Fig. 2). There was also evidence of ethmoid and frontal sinusitis. He was admitted to the hospital with a diagnosis of periorbital cellulitis and sinusitis (Fig. 3) and started on intravenous vancomycin and clindamycin. Despite treatment with broad-spectrum antibiotics, including ampicillin-sulbactam, vancomycin, and clindamycin, the patient’s condition rapidly progressed to significant edema and erythema of the right periorbital tissue and forehead, with increased intraorbital pressure, diplopia, and dilated pupil unresponsive to light on the right. Extraocular movements were decreased, and the patient had pain with upward and lateral gaze. Visual acuity was decreased to 2-finger discrimination. Surgical exploration performed within 24 hours of admission revealed necrotic fascia and periosteum. Lateral canthotomy with inferior cantholysis and extensive soft tissue debridement
FIG. 1. Patient at time of initial surgical debridement. Note the erythema and edema of forehead and right periorbital region.
© 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
e31
Ophthal Plast Reconstr Surg, Vol. 31, No. 2, 2015
Case Reports
After serial debridements and intravenous broad-spectrum antibiotic treatment, the edema and erythema improved, and visual acuity was restored. The patient was discharged home on intravenous ampicillin/sulbactam and clindamycin and continued to improve on an outpatient basis. Ultimately, given the gross and pathologic findings, it was believed that the patient’s condition began as an ethmoid sinusitis that progressed to orbital necrotizing fasciitis and osteomyelitis.
DISCUSSION
FIG. 2. CT orbit demonstrating gas in the soft tissue adjacent to the frontal sinus.
FIG. 3. CT orbit demonstrating periorbital gas and sinusitis.
including deep fascia, periosteum, medial orbital wall, and ethmoidal mucosa was performed along with medial orbital wall decompression to relieve increased intraorbital pressure and to decompress the optic nerve. Wounds were left open, and drains were placed. The patient was kept on intravenous antibiotics, and 3 additional debridements were required over the following 5 days. Presence of necrotic orbital periosteum and necrotic orbital roof was noted at each debridement. Wounds were eventually closed in a delayed fashion. The initial surgical pathologic study report revealed no specific organisms but demonstrated osteomyelitis of the right orbital wall, periorbital cellulitis, and acute and chronic sinusitis. Microbiology specimens were sent to the Texas Department of State Health Services for further identification, and results revealed Arcanobacterium haemolyticum.
e32
Our patient presented with orbital necrotizing fasciitis and osteomyelitis due to Arcanobacterium haemolyticum, which represents a unique case of a potentially l ife-threatening infection caused by a rare pathogen. Typically, organisms causing necrotizing fasciitis of the head and neck include β-hemolytic Streptococcal species and Staphyloccocus aureus. Complications include extensive soft tissue loss, causing disfigurement, permanent blindness, septic shock, and death, with mortality rates reported as high as 76%.5 The rapidly progressive and potentially life-threatening nature of this infection underscores the importance of early diagnosis and treatment. Prompt diagnosis of this condition is challenging, as its early presentation is similar to sinusitis or cellulitis. To properly diagnose necrotizing fasciitis, high clinical suspicion and close observation for rapidly developing signs and symptoms are necessary. CT scanning is the most useful diagnostic study, revealing inflammation and gas production along fascial planes in areas inaccessible to direct palpation and thus difficult to recognize on physical examination. Aggressive surgical debridement is generally accepted as the most important intervention in cases of necrotizing fasciitis. Surgical intervention is indicated in cases of rapidly progressing symptoms and presence of perifascial gas visualized by CT scan. Serial debridements are recommended to prevent the spread of this devastating type of infection. Though there have been reports of successful conservative treatment of necrotizing fasciitis,6,7 we tend to agree with Bingöl-Koloğlu8 that, in general, nonoperative treatment is a highly controversial and unsafe approach. Treatment of necrotizing fasciitis with broad-spectrum antibiotics should be used as an adjunct to primary surgical debridement. Empiric antibiotic treatment should include penicillin, clindamycin, and an aminoglycoside to cover gram positives and clostridia, anaerobes, and gram negatives, respectively. Antibiotic therapy should be tailored to identify putative organism(s) whenever possible to prevent resistance. Arcanobacterium haemolyticum orbital necrotizing fasciitis and osteomyelitis has not been described, though Arcanobacterium haemolyticum orbital cellulitis with subperiosteal abscess and sinusitis has been reported.1,2 Arcanobacterium haemolyticum is also a rare cause of multiple other infections9,10 including necrotizing fasciitis of the lower extremity.3 Arcanobacterium haemolyticum most commonly causes pharyngitis, particularly in the pediatric population.4 However, the overall incidence of Arcanobacterium haemolyticum pharyngitis is very low. Systemic infections are not commonly seen.9 Though the epidemiology of Arcanobacterium haemolyticum infection has not been well documented, Arcanobacterium haemolyticum infections tend to occur in adolescents or immunosupressed adults, including diabetics. Humans are thought to be the natural reservoir.9 Interspecies transmission has been suggested with infection possibly linked to livestock exposure. Coinfection may also be a significant mechanism promoting pathogenicity. The optimum antibiotic therapy for Arcanobacterium haemolyticum infections has yet to be established by the literature. However, a few studies report on the efficacy of different antibiotic regimens used to treat Arcanobacterium haemolyticum
© 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
Ophthal Plast Reconstr Surg, Vol. 31, No. 2, 2015
infections. The most common antibiotic regimens include a combination of β lactams plus an aminoglycoside for soft tissue infections, whereas rifampicin or clindamycin may be considered in the treatment of deep-seated infections like osteomyelitis.10 A study by Carlson et al.11 evaluated the antimicrobial susceptibility of 138 clinical isolates of Arcanobacterium haemolyticum. This study found that all isolates were susceptible to phenoxymethylpenicillin, cephalopsporins, erythromycin, azithromycin, clindamycin, vancomycin, doxycycline, and ciprofloxacin but were resistant to trimethoprim-sulfamethoxazole. Resistance to tetracyclines has also been reported.1
CONCLUSIONS Arcanobacterium haemolyticum is a rare but significant cause of orbital necrotizing fasciitis. Improvements in pathogen identification and awareness of the potential role of Arcanobacterium haemolyticum in orbital necrotizing fasciitis may improve the efficiency of diagnosis and treatment and avoid the potentially devastating complications of this infection.
REFERENCES 1. Limjoco-Antonio AD, Janda WM, Schreckenberger PC. Arcanobacterium haemolyticum sinusitis and orbital cellulitis. Pediatr Infect Dis J 2003;22:465–7. 2. Ford JG, Yeatts RP, Givner LB. Orbital cellulitis, subperiosteal abscess, sinusitis, and septicemia caused b Arcanobacterium haemolyticum. Am J Ophthalmol 1995;120:261–2. 3. Lee S, Roh KH, Kim CK, et al. A case of necrotizing fasciitis due to Streptococcus agalactiae, Arcanobacterium haemolyticum, and Finegoldia magna in a dog-bitten patient with diabetes. Korean J Lab Med 2008;28:191–5. 4. Mackenzie A, Fuite LA, Chan FT, et al. Incidence and pathogenicity of Arcanobacterium haemolyticum during a 2-year study in Ottawa. Clin Infect Dis 1995;21:177–81. 6. Wakhlu A, Chaudhary A, Tandon RK, et al. Conservative management of necrotizing fascitis in children. J Pediatr Surg 2006;41:1144–8. 7. Norrby-Teglund A, Muller MP, Mcgeer A, et al. Successful management of severe group A streptococcal soft tissue infections using an aggressive medical regimen including intravenous polyspecific immunoglobulin together with a conservative surgical approach. Scand J Infect Dis 2005;37:166–72. 8. Bingöl-Koloğlu M, Yildiz RV, Alper B, et al. Necrotizing fasciitis in children: diagnostic and therapeutic aspects. J Pediatr Surg 2007;42:1892–7. 9. Parija SC, Kaliaperumal V, Kumar SV, et al. Arcanobacterium haemolyticum associated with pyothorax: case report. BMC Infect Dis 2005;5:68. 10. Tan TY, Ng SY, Thomas H, et al. Arcanobacterium haemolyticum bacteraemia and soft-tissue infections: case report and review of the literature. J Infect 2006;53:e69–74. 11. Carlson P, Korpela J, Walder M, et al. Antimicrobial susceptibilities and biotypes of Arcanobacterium haemolyticum blood isolates. Eur J Clin Microbiol Infect Dis 1999;18:915–7.
Naphazoline as a Confounder in the Diagnosis of Carotid Artery Dissection John D. Pemberton, D.O.*†, Peter W. MacIntosh, M.D.‡, Ahmaida Zeglam, B.B.A*, and Aaron Fay, M.D.‡§ Abstract: Diagnosing Horner Syndrome can be difficult in the setting of an incomplete triad. A 27-year-old man presented with unilateral eyelid droop and intermittent ipsilateral headaches, having already seen 7 physicians. Physical examination revealed unilateral ptosis but no
Case Reports
pupillary miosis or facial anhidrosis. Inspection of his clinical photographs revealed elevation of the ipsilateral lower eyelid, suggesting sympathetic dysfunction. On further questioning, he admitted to naphazoline dependence. Reexamination after ceasing the naphazoline unveiled the anisocoria. Vascular imaging subsequently revealed carotid dissection, and the patient was started on anticoagulant and antiplatelet therapy. The ptosis persisted after conjunctival Müllerectomy. External levator resection was recommended, but patient declined. This case underscores the importance of clinical photography, meticulous medical record review, and complete medication history including over-the-counter preparations. Clinicians should meticulously inspect the lower eyelid in cases of atypical blepharoptosis and consider the effects of eye drops when inspecting pupils for miosis.
C
haracterized by the triad of unilateral miosis, facial anhidrosis, and mild upper eyelid ptosis, Horner syndrome represents the most important neuro-ophthalmic cause of a pupil that dilates poorly in the dark.1 The syndrome occurs secondary to interruption of the oculosympathetic pathway that originates in the hypothalamus, descends in the neck to the apex of the lung, then reverses direction to ascend along the internal carotid artery to terminate in various sympathetically innervated structures including the iris dilator muscle and Müller’s muscle. A lesion at any level along this pathway can cause Horner syndrome; common etiologies include congenital anomaly, lateral medullary stroke, Pancoast tumor, and carotid dissection. Although the Horner triad is well engrained in the minds of ophthalmologists, the diagnosis can be elusive if any of the clinical findings is subtle, absent, or masked by other processes. Naphazoline hydrochloride is a direct-acting sympathomimetic that is a common component in a myriad of topical ophthalmic antihistamines and decongestants. This medication is reported to cause conjunctival vasoconstriction, mydriasis, blurred vision, and irritation.2 This report, prepared in accordance with the Health Insurance Portability and Accountability Act of 1996 Privacy Rule, describes a case of Horner syndrome due to carotid dissection with miosis and ptosis masked by naphazoline use. The incomplete clinical findings of Horner syndrome lead to a delay in the diagnosis of the patient’s carotid dissection.
CASE DESCRIPTION A 27-year-old man presented to his primary care physician with a 2-month history of a droopy left upper eyelid, OS pain with conjunctival injection, and intermittent unilateral headaches. He did not complain of asymmetry of facial sweating. His symptoms improved with the use of Visine A. He had no significant medical or ocular history and no history of trauma or chiropractic manipulation. He was taking no additional medications. He had no known drug allergies, smoked 1 pack of cigarettes per month, and drank alcohol socially. Accepted for publication September 24, 2013. *College of Medicine Division, University of Arkansas for Medical Sciences; †Department of Ophthalmology, Jones Eye Institute at the University of Arkansas for Medical Sciences, Little Rock, Arkansas; ‡Department of Ophthalmology, Harvard Medical School; and §Department of Ophthalmology, Ophthalmic Plastic and Reconstructive Surgery, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, U.S.A. The authors have no financial or conflicts of interest to disclose. Address correspondence and reprint requests to Aaron Fay, M.D., Massachusetts Eye and Ear Infirmary, 243 Charles St., Boston, MA 02114. E-mail: [email protected] DOI: 10.1097/IOP.0000000000000059
© 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
e33
Orbital Necrotizing Fasciitis and Osteomyelitis Caused by Arcanobacterium Haemolyticum: A Case Report Lindsay A. Stone, M.D., M.Sc.*, and Raymond J. Harshbarger III, M.D., F.A.C.S., F.A.A.P.† Abstract: The facial region is infrequently affected by necrotizing infections. Orbital necrotizing infections are even rarer, seen following trauma, local skin infection, and sinusitis. The authors report a unique case of orbital necrotizing fasciitis and osteomyelitis resulting from Arcanobacterium Haemolyticum ethmoid sinusitis. No prior occurrences of Arcanobacterial species orbital necrotizing fasciitis/osteomyelitis have been reported. A 16-year-old boy presented to the ER with a 3-day history of fever, chills, headache, and sinus pressure. CT scan revealed soft tissue swelling of the right orbit, forehead, and ethmoid sinusitis. Within 24 hours of admission, he suffered rapidly progressive swelling and erythema of the right orbit and forehead with diminished visual acuity, despite broad-spectrum antibiotics. Orbital exploration revealed frankly necrotic fascia and periosteum along the superior aspect. Lateral canthotomy, cantholysis, decompression of the optic nerve, and soft tissue debridement with bone biopsy was performed. Operative specimens isolated Arcanobacterium Haemolyticum. Pathologic examination revealed right orbital osteomyelitis.
N
ecrotizing fasciitis is a deep soft tissue infection with a predilection for the fascial layers. Tissue destruction is rapidly progressive and therefore requires timely diagnosis and treatment. Treatment of necrotizing fasciitis of any etiology necessitates aggressive tissue debridement and initiation of broad-spectrum antibiotics. Arcanobacterium haemolyticum has been implicated as a causal agent in infections including orbital cellulitis and sinusitis,1,2 necrotizing fasciitis of the extremity,3 osteomyelitis, wound infection, and abscess. Arcanobacterium haemolyticum can also be found as normal human flora and is often isolated in combination with other pathogens. Though most commonly implicated as a cause of pharyngitis4 in the pediatric population, the incidence is still rare. Diagnosis and treatment of Arcanobacterium haemolyticum infections can be challenging due to their relative infrequency. Furthermore, many laboratories do not routinely culture for Arcanobacterium haemolyticum, thus contributing to unrecognized infections or delays in diagnosis. However, there is no consensus regarding the optimal antibiotic treatment regimen for Arcanobacterium haemolyticum infections. The authors present a case of orbital necrotizing fasciitis with osteomyelitis caused by Arcanobacterium haemolyticum in an otherwise healthy adolescent male. Necrotizing fasciitis of the face is relatively uncommon, and a case of orbital necrotizing fasciitis with osteomyelitis secondary to Arcanobacterium haemolyticum has not been reported to the best of our knowledge. This case study was conducted in full compliance with
Accepted for publication August 30, 2013. *Oregon Health & Science University, Portland; †Craniofacial & Pediatric Plastic Surgery, Dell Children’s Medical Center of Central Texas, University Medical Center at Brackenridge, Austin, Texas, U.S.A. The authors have no financial or conflict of interest to disclose. Address correspondence and reprint requests to Raymond J. Harshbarger, III, M.D., F.A.C.S., F.A.A.P., Craniofacial & Pediatric Plastic Surgery, Dell Children’s Medical Center of Central Texas, University Medical Center at Brackenridge, Austin, TX 78723. E-mail: [email protected] DOI: 10.1097/IOP.0000000000000057
Case Reports
Health Insurance Portability and Accountability Act guidelines, and patient consent for the use of photography was obtained. Objective. To draw attention to a rare but significant pathogen as the etiologic factor in orbital necrotizing fasciitis.
CASE DESCRIPTION A 16-year-old man without significant medical history presented to the ER with a 4-day history of OD pain, swelling, nasal congestion, chills, headache, and sinus pain. He denied any recent trauma to the eye. The patient denied regular use of medication, had no known drug allergies, and was up to date on immunizations. He had presented to an outside ER the previous day, but after a negative workup for Strep throat and influenza, he was given prochlorperazine and discharged home. Physical examination revealed a drowsy but arousable adolescent man with right-sided periorbital swelling and erythema, proptosis, and decreased extraocular movements on the right (Fig. 1). Laboratory investigations on admission showed a white blood cell count of 19.9 × 103 cells/μL, 64% neutrophils, and bandemia with 26% band cells. A CT of the orbit demonstrated swelling in the right frontal and periorbital regions with air densities adjacent to the right frontal sinus (Fig. 2). There was also evidence of ethmoid and frontal sinusitis. He was admitted to the hospital with a diagnosis of periorbital cellulitis and sinusitis (Fig. 3) and started on intravenous vancomycin and clindamycin. Despite treatment with broad-spectrum antibiotics, including ampicillin-sulbactam, vancomycin, and clindamycin, the patient’s condition rapidly progressed to significant edema and erythema of the right periorbital tissue and forehead, with increased intraorbital pressure, diplopia, and dilated pupil unresponsive to light on the right. Extraocular movements were decreased, and the patient had pain with upward and lateral gaze. Visual acuity was decreased to 2-finger discrimination. Surgical exploration performed within 24 hours of admission revealed necrotic fascia and periosteum. Lateral canthotomy with inferior cantholysis and extensive soft tissue debridement
FIG. 1. Patient at time of initial surgical debridement. Note the erythema and edema of forehead and right periorbital region.
© 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
e31
Ophthal Plast Reconstr Surg, Vol. 31, No. 2, 2015
Case Reports
After serial debridements and intravenous broad-spectrum antibiotic treatment, the edema and erythema improved, and visual acuity was restored. The patient was discharged home on intravenous ampicillin/sulbactam and clindamycin and continued to improve on an outpatient basis. Ultimately, given the gross and pathologic findings, it was believed that the patient’s condition began as an ethmoid sinusitis that progressed to orbital necrotizing fasciitis and osteomyelitis.
DISCUSSION
FIG. 2. CT orbit demonstrating gas in the soft tissue adjacent to the frontal sinus.
FIG. 3. CT orbit demonstrating periorbital gas and sinusitis.
including deep fascia, periosteum, medial orbital wall, and ethmoidal mucosa was performed along with medial orbital wall decompression to relieve increased intraorbital pressure and to decompress the optic nerve. Wounds were left open, and drains were placed. The patient was kept on intravenous antibiotics, and 3 additional debridements were required over the following 5 days. Presence of necrotic orbital periosteum and necrotic orbital roof was noted at each debridement. Wounds were eventually closed in a delayed fashion. The initial surgical pathologic study report revealed no specific organisms but demonstrated osteomyelitis of the right orbital wall, periorbital cellulitis, and acute and chronic sinusitis. Microbiology specimens were sent to the Texas Department of State Health Services for further identification, and results revealed Arcanobacterium haemolyticum.
e32
Our patient presented with orbital necrotizing fasciitis and osteomyelitis due to Arcanobacterium haemolyticum, which represents a unique case of a potentially l ife-threatening infection caused by a rare pathogen. Typically, organisms causing necrotizing fasciitis of the head and neck include β-hemolytic Streptococcal species and Staphyloccocus aureus. Complications include extensive soft tissue loss, causing disfigurement, permanent blindness, septic shock, and death, with mortality rates reported as high as 76%.5 The rapidly progressive and potentially life-threatening nature of this infection underscores the importance of early diagnosis and treatment. Prompt diagnosis of this condition is challenging, as its early presentation is similar to sinusitis or cellulitis. To properly diagnose necrotizing fasciitis, high clinical suspicion and close observation for rapidly developing signs and symptoms are necessary. CT scanning is the most useful diagnostic study, revealing inflammation and gas production along fascial planes in areas inaccessible to direct palpation and thus difficult to recognize on physical examination. Aggressive surgical debridement is generally accepted as the most important intervention in cases of necrotizing fasciitis. Surgical intervention is indicated in cases of rapidly progressing symptoms and presence of perifascial gas visualized by CT scan. Serial debridements are recommended to prevent the spread of this devastating type of infection. Though there have been reports of successful conservative treatment of necrotizing fasciitis,6,7 we tend to agree with Bingöl-Koloğlu8 that, in general, nonoperative treatment is a highly controversial and unsafe approach. Treatment of necrotizing fasciitis with broad-spectrum antibiotics should be used as an adjunct to primary surgical debridement. Empiric antibiotic treatment should include penicillin, clindamycin, and an aminoglycoside to cover gram positives and clostridia, anaerobes, and gram negatives, respectively. Antibiotic therapy should be tailored to identify putative organism(s) whenever possible to prevent resistance. Arcanobacterium haemolyticum orbital necrotizing fasciitis and osteomyelitis has not been described, though Arcanobacterium haemolyticum orbital cellulitis with subperiosteal abscess and sinusitis has been reported.1,2 Arcanobacterium haemolyticum is also a rare cause of multiple other infections9,10 including necrotizing fasciitis of the lower extremity.3 Arcanobacterium haemolyticum most commonly causes pharyngitis, particularly in the pediatric population.4 However, the overall incidence of Arcanobacterium haemolyticum pharyngitis is very low. Systemic infections are not commonly seen.9 Though the epidemiology of Arcanobacterium haemolyticum infection has not been well documented, Arcanobacterium haemolyticum infections tend to occur in adolescents or immunosupressed adults, including diabetics. Humans are thought to be the natural reservoir.9 Interspecies transmission has been suggested with infection possibly linked to livestock exposure. Coinfection may also be a significant mechanism promoting pathogenicity. The optimum antibiotic therapy for Arcanobacterium haemolyticum infections has yet to be established by the literature. However, a few studies report on the efficacy of different antibiotic regimens used to treat Arcanobacterium haemolyticum
© 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
Ophthal Plast Reconstr Surg, Vol. 31, No. 2, 2015
infections. The most common antibiotic regimens include a combination of β lactams plus an aminoglycoside for soft tissue infections, whereas rifampicin or clindamycin may be considered in the treatment of deep-seated infections like osteomyelitis.10 A study by Carlson et al.11 evaluated the antimicrobial susceptibility of 138 clinical isolates of Arcanobacterium haemolyticum. This study found that all isolates were susceptible to phenoxymethylpenicillin, cephalopsporins, erythromycin, azithromycin, clindamycin, vancomycin, doxycycline, and ciprofloxacin but were resistant to trimethoprim-sulfamethoxazole. Resistance to tetracyclines has also been reported.1
CONCLUSIONS Arcanobacterium haemolyticum is a rare but significant cause of orbital necrotizing fasciitis. Improvements in pathogen identification and awareness of the potential role of Arcanobacterium haemolyticum in orbital necrotizing fasciitis may improve the efficiency of diagnosis and treatment and avoid the potentially devastating complications of this infection.
REFERENCES 1. Limjoco-Antonio AD, Janda WM, Schreckenberger PC. Arcanobacterium haemolyticum sinusitis and orbital cellulitis. Pediatr Infect Dis J 2003;22:465–7. 2. Ford JG, Yeatts RP, Givner LB. Orbital cellulitis, subperiosteal abscess, sinusitis, and septicemia caused b Arcanobacterium haemolyticum. Am J Ophthalmol 1995;120:261–2. 3. Lee S, Roh KH, Kim CK, et al. A case of necrotizing fasciitis due to Streptococcus agalactiae, Arcanobacterium haemolyticum, and Finegoldia magna in a dog-bitten patient with diabetes. Korean J Lab Med 2008;28:191–5. 4. Mackenzie A, Fuite LA, Chan FT, et al. Incidence and pathogenicity of Arcanobacterium haemolyticum during a 2-year study in Ottawa. Clin Infect Dis 1995;21:177–81. 6. Wakhlu A, Chaudhary A, Tandon RK, et al. Conservative management of necrotizing fascitis in children. J Pediatr Surg 2006;41:1144–8. 7. Norrby-Teglund A, Muller MP, Mcgeer A, et al. Successful management of severe group A streptococcal soft tissue infections using an aggressive medical regimen including intravenous polyspecific immunoglobulin together with a conservative surgical approach. Scand J Infect Dis 2005;37:166–72. 8. Bingöl-Koloğlu M, Yildiz RV, Alper B, et al. Necrotizing fasciitis in children: diagnostic and therapeutic aspects. J Pediatr Surg 2007;42:1892–7. 9. Parija SC, Kaliaperumal V, Kumar SV, et al. Arcanobacterium haemolyticum associated with pyothorax: case report. BMC Infect Dis 2005;5:68. 10. Tan TY, Ng SY, Thomas H, et al. Arcanobacterium haemolyticum bacteraemia and soft-tissue infections: case report and review of the literature. J Infect 2006;53:e69–74. 11. Carlson P, Korpela J, Walder M, et al. Antimicrobial susceptibilities and biotypes of Arcanobacterium haemolyticum blood isolates. Eur J Clin Microbiol Infect Dis 1999;18:915–7.
Naphazoline as a Confounder in the Diagnosis of Carotid Artery Dissection John D. Pemberton, D.O.*†, Peter W. MacIntosh, M.D.‡, Ahmaida Zeglam, B.B.A*, and Aaron Fay, M.D.‡§ Abstract: Diagnosing Horner Syndrome can be difficult in the setting of an incomplete triad. A 27-year-old man presented with unilateral eyelid droop and intermittent ipsilateral headaches, having already seen 7 physicians. Physical examination revealed unilateral ptosis but no
Case Reports
pupillary miosis or facial anhidrosis. Inspection of his clinical photographs revealed elevation of the ipsilateral lower eyelid, suggesting sympathetic dysfunction. On further questioning, he admitted to naphazoline dependence. Reexamination after ceasing the naphazoline unveiled the anisocoria. Vascular imaging subsequently revealed carotid dissection, and the patient was started on anticoagulant and antiplatelet therapy. The ptosis persisted after conjunctival Müllerectomy. External levator resection was recommended, but patient declined. This case underscores the importance of clinical photography, meticulous medical record review, and complete medication history including over-the-counter preparations. Clinicians should meticulously inspect the lower eyelid in cases of atypical blepharoptosis and consider the effects of eye drops when inspecting pupils for miosis.
C
haracterized by the triad of unilateral miosis, facial anhidrosis, and mild upper eyelid ptosis, Horner syndrome represents the most important neuro-ophthalmic cause of a pupil that dilates poorly in the dark.1 The syndrome occurs secondary to interruption of the oculosympathetic pathway that originates in the hypothalamus, descends in the neck to the apex of the lung, then reverses direction to ascend along the internal carotid artery to terminate in various sympathetically innervated structures including the iris dilator muscle and Müller’s muscle. A lesion at any level along this pathway can cause Horner syndrome; common etiologies include congenital anomaly, lateral medullary stroke, Pancoast tumor, and carotid dissection. Although the Horner triad is well engrained in the minds of ophthalmologists, the diagnosis can be elusive if any of the clinical findings is subtle, absent, or masked by other processes. Naphazoline hydrochloride is a direct-acting sympathomimetic that is a common component in a myriad of topical ophthalmic antihistamines and decongestants. This medication is reported to cause conjunctival vasoconstriction, mydriasis, blurred vision, and irritation.2 This report, prepared in accordance with the Health Insurance Portability and Accountability Act of 1996 Privacy Rule, describes a case of Horner syndrome due to carotid dissection with miosis and ptosis masked by naphazoline use. The incomplete clinical findings of Horner syndrome lead to a delay in the diagnosis of the patient’s carotid dissection.
CASE DESCRIPTION A 27-year-old man presented to his primary care physician with a 2-month history of a droopy left upper eyelid, OS pain with conjunctival injection, and intermittent unilateral headaches. He did not complain of asymmetry of facial sweating. His symptoms improved with the use of Visine A. He had no significant medical or ocular history and no history of trauma or chiropractic manipulation. He was taking no additional medications. He had no known drug allergies, smoked 1 pack of cigarettes per month, and drank alcohol socially. Accepted for publication September 24, 2013. *College of Medicine Division, University of Arkansas for Medical Sciences; †Department of Ophthalmology, Jones Eye Institute at the University of Arkansas for Medical Sciences, Little Rock, Arkansas; ‡Department of Ophthalmology, Harvard Medical School; and §Department of Ophthalmology, Ophthalmic Plastic and Reconstructive Surgery, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, U.S.A. The authors have no financial or conflicts of interest to disclose. Address correspondence and reprint requests to Aaron Fay, M.D., Massachusetts Eye and Ear Infirmary, 243 Charles St., Boston, MA 02114. E-mail: [email protected] DOI: 10.1097/IOP.0000000000000059
© 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
e33
