Photograph of the patient showing a granulated postauricular incision with erythema and drainage 14 days after face-lift surgery.
Brain magnetic resonance imaging studies. A, Two-dimensional time-of-flight magnetic resonance venogram (lateral view) demonstrates loss of flow signal in the anterior and mid segments of the superior sagittal sinus (arrows). B, Coronal contrast-enhanced T1-weighted image reveals a large, enhancing left curvilinear subdural empyema (arrows) and signal loss (darkening) in the superior sagittal sinus (arrowhead), consistent the presence of sinus thrombus. C, Axial contrast-enhanced T1-weighted image demonstrates extensive left frontotemporal skin and subcutaneous soft-tissue swelling with abnormal enhancement. D, Axial T2-weighted image demonstrates large, left greater than right cerebral venous and arterial infarctions and edema.
Sifri CD, Solenski N. Fatal Septic Thrombosis of the Superior Sagittal Sinus After Face-lift Surgery Caused by Community-Associated Methicillin-Resistant Staphylococcus aureus. Arch Facial Plast Surg. 2009;11(2):140-147. doi:10.1001/archfacial.2008.522
A recent report by Zoumalan and Rosenberg1 highlighted the importance of methicillin-resistant Staphylococcus aureus (MRSA) in postoperative wound infection after rhytidectomy. In their study, MRSA was isolated in 4 of 5 patients with surgical site infections after face-lift surgery. Two of the 4 patients required hospitalization for wound care and parenteral antibiotics to cure the infection, whereas the other 2 patients with MRSA wound infections were treated with local care and oral antibiotics as outpatients. Fortunately, prompt treatment with surgical drainage and antibiotic therapy guided by susceptibility testing resulted in excellent outcomes in all patients. It stands to reason, however, that delayed recognition or inappropriate treatment of these infections may not have led to such favorable results. Herein, we report an additional case of surgical site infection following rhytidectomy caused by an epidemic community-associated (CA) strain of MRSA that unfortunately had a delayed diagnosis and tragic outcome.
In March 2008, a 53-year-old woman was admitted to the intensive care unit with fever, vomiting, obtundation, and a granulated left postauricular scalp incision 6 weeks after undergoing rhytidectomy. The patient had been given a course of cephalexin for preoperative antibiotic prophylaxis 2 weeks prior to surgery. She underwent eyebrow-lift surgery followed by rhytidectomy 5 days later. Two weeks after face-lift surgery, the patient developed swelling, erythema, and tenderness along the postauricular surgical incision extending around the left ear and down the anterior aspect of the neck (Figure 1). The wound partially separated and produced bloody drainage. After 2 additional courses of cephalexin, erythema and induration improved but were still evident anterior and posterior to the ear. The surgical wound closed, but the patient continued to experience pain and occasional drainage along the incision. Culture samples of the drainage were not obtained during this time. Two days before admission, she developed a severe headache followed by nausea, vomiting, and photophobia a day later. On the day of admission, she became acutely confused, combative, and lethargic, and was transported by helicopter to our hospital.
She had no history of prior skin or soft-tissue infections, use of alcohol or illicit drugs, or recent health care exposure. She was hepatitis C virus positive but had no history of liver dysfunction. Results of human immunodeficiency virus antibody tests before and during the hospitalization were negative. She worked as a licensed manicurist and masseuse.
On arrival, she had a temperature of 41.0°C, a heart rate of 118 beats/min, and blood pressure of 148/81 mm Hg. She was intubated and minimally responsive. Neurological examination revealed a left sixth cranial nerve palsy, paralysis of the right upper extremity, 3+ deep tendon reflexes, and bilateral Babinski signs. The left eye was chemotic but not proptotic. The remainder of the examination was notable for nuchal rigidity and bilateral pulmonary crackles. Treatment with vancomycin hydrochloride, ceftriaxone, and acyclovir was started. Laboratory studies revealed that her white blood cell (WBC) count was 13100/μL; erythrocyte sedimentation rate, 84 mm/h; and C-reactive protein level higher than 100 mg/L. Cerebrospinal fluid (CSF) examination revealed a leukocyte count of 266/μL (96% segmented neutrophils); protein level, 249 mg/dL; lactate level, 39.64 mg/dL; and a glucose level within reference range. (To convert WBC count to times 109 per liter, multiply by 0.001; to convert C-reactive protein to nanomoles per liter, multiply by 9.524; to convert lactate to millimoles per liter, multiply by 0.111.) Magnetic resonance imaging and venography of the patient's head demonstrated thrombosis of the anterior and mid-superior sagittal sinus, multiple venous infarcts, prominent leptomeningeal enhancement, and a left subdural fluid collection (Figure 2). Blood cultures taken at the time of admission yielded MRSA, and therapy was adjusted to vancomycin, rifampin, and heparin sodium. Vancomycin trough concentrations were maintained at 20 to 25 μg/mL. The patient underwent emergency decompressive bifrontal craniectomy with debridement of epidural and subdural intracerebral empyemas. Purulent fluid was also evacuated from the subgaleal space. Cultures of the CSF, dura, skull, and thrombosed sagittal sinus all yielded MRSA. Unfortunately, the patient remained neurologically devastated despite decompressive surgery, and follow-up imaging showed the development of frontal lobe intraparenchymal abscesses, multiple septic pulmonary emboli, and evolving bihemispheric strokes. The family decided to focus her care on comfort measures only, and she died on hospital day 23. Autopsy findings confirmed bilateral frontal lobe infarctions and abscesses, extensive meningitis, superior sagittal sinus thrombosis, and diffuse bronchopneumonia with abscess formation.
The S aureus isolates obtained from blood, lung, and central nervous system (skull, subdural, and thrombosed superior sagittal sinus) cultures had identical antibiotic susceptibility profiles as follows:
Molecular analysis of representative isolates was performed as previously described.2 Methicillin resistance was confirmed by polymerase chain reaction of the mecA gene and by the PBP2a Latex Agglutination test (Oxoid, Hampshire, England). The isolates had a pulse field gel electrophoresis profile identical to the epidemic CA-MRSA clone USA300-0114. Further molecular analysis demonstrated that the isolates contained other elements characteristic of epidemic CA-MRSA USA300, including the Panton-Valentine leukocidin genes lukSF-PV and the arginine catabolic mobile element.
The past decade has witnessed the worldwide emergence and epidemic spread of CA-MRSA strains that are genotypically and phenotypically distinct from traditional hospital-associated (HA) strains.3 For example, a recent study4 found that MRSA was the most common (in 59% of cases) cause of purulent skin and soft-tissue infections in patients presenting in US emergency departments. Most isolates (97%) belonged to a single CA-MRSA clonal type, termed USA300; 1 remarkably successful subtype, termed USA300-0114 (the clone identified in this case), accounted for 74% of those cases. Furthermore, CA-MRSA is increasingly found to be a cause of surgical site infections, even in patients undergoing same-day surgery.5 Presumably, most ambulatory surgery patients who develop CA-MRSA wound infections were asymptomatically colonized at the time of surgery. Although CA-MRSA is usually associated with soft-tissue infections, it can also cause highly invasive and potentially lethal infections, including necrotizing pneumonia, septic cavernous sinus thrombosis, and pyogenic brain abscess.2,6- 8 The fulminant nature of these unusual cases has led many investigators to speculate that CA-MRSA may be more virulent than HA-MRSA.3 In fact, CA-MRSA strains have been shown to be more virulent than HA-MRSA in neutrophil survival and murine infection studies9; however, the factors that may make CA-MRSA more virulent or transmissible have not yet been clearly defined.
Herein, we present a case of surgical site infection after face-lift surgery caused by the epidemic strain of CA-MRSA USA300. At least 1 of the cases of MRSA face-lift wound infection described by Zoumalan and Rosenberg1 was also likely caused by a CA-MRSA strain based on the antibiotic susceptibility pattern of the isolate, but molecular analysis was not performed. To our knowledge, this is the first report of death attributable to an infection complicating face-lift surgery and the first fatal case of septic dural sinus thrombosis caused by CA-MRSA. In the preantibiotic era, uncontrolled infections of the face were a common cause of septic dural sinus thromboses, and mortality rates of these now-rare conditions remain high in the modern era (30% for septic cavernous sinus thrombosis, 78% for septic sagittal sinus thrombosis).10
The emergence of MRSA as a CA pathogen will likely be an ongoing challenge in the care of ambulatory surgery patients.1,5 All MRSA wound infections should be treated aggressively with surgical drainage and appropriate antibiotic therapy.1,3 A recent study11 reporting a higher than 90% cure rate of uncomplicated CA-MRSA skin abscesses with incision and drainage combined with either a placebo or an antibiotic predicted to be ineffective (cephalexin) is yet another clear demonstration of the primacy of surgical drainage in the treatment of these infections. Less clear and in need of study are the optimal methods to identify, treat, and prevent disease in ambulatory patients at risk for MRSA surgical site infections. In conclusion, emergence of MRSA within the community represents a clear and present danger to individuals traditionally considered to be at low risk for MRSA infection, including those undergoing ambulatory surgical procedures.
Correspondence: Dr Sifri, Division of Infectious Diseases and International Health, University of Virginia Health System, PO Box 801361, Charlottesville, VA 22908-1361 (firstname.lastname@example.org).
Author Contributions:Study concept and design: Sifri and Solenski. Acquisition of data: Sifri and Solenski. Analysis and interpretation of data: Sifri and Solenski. Drafting of the manuscript: Sifri and Solenski. Critical revision of the manuscript for important intellectual content: Sifri and Solenski. Administrative, technical, and material support: Sifri.
Financial Disclosure: None reported.
Funding/Support: Work in the Sifri Laboratory is supported by a Howard Hughes Medical Institute Early Career Award.
Additional Contributions: Ann Karen Brassinga, PhD, and Meghan Cupp, BS, provided technical assistance.