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* From the Departments of Regional Practice Anesthesiology Hillcrest Hospital, Mayfield Heights; and
Obstetric Anesthesiology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA.
Address correspondence to: Dr. Kenneth C. Cummings III, Department of Anesthesiology, Hillcrest Hospital, 6780 Mayfield Road, Mayfield Heights, Ohio 44124, USA. Phone: 440-312-3022; Fax: 440-312-6963; E-mail: cummink2{at}ccf.org
| Abstract |
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Clinical Features: A 33 yr-old gravida 2 nulliparous patient at 36 weeks gestation presented with severe pre-eclampsia, and PUPPP (treated with prednisone). Magnesium prophylaxis was started and labour was induced. An epidural catheter was placed at the L3-4 level using standard aseptic technique. Bupivacaine was incrementally injected to achieve a T10 sensory level, and analgesia was maintained using a continuous infusion of 0.0625% bupivacaine with fentanyl. Nine days post-delivery, the patient developed back pain radiating to her right leg, but she was otherwise asymptomatic. She was afebrile; with a slightly tender, non-erythematous, non-draining, 1 cm nodule at the epidural catheter site. Motor and sensory examinations were normal at that time. However, the patient returned 24 hr later and further investigations revealed: WBC 17,800·mm3, platelets 486,000·mm3, erythrocyte sedimentation rate 50 mm·hr1, and C-reactive protein 8.8 mg·dL1. The magnetic resonance imaging demonstrated an EA at the L3-4 level causing minimal cord compression. The patient underwent an emergency decompressive laminectomy. Cultures revealed methicillin-sensitive Staphylococcus aureus. Her pain improved, and she was discharged on the third postoperative day with a six-week course of iv ceftriaxone.
Conclusion: Causative organisms for EAs include coagulase-negative Staphylococci, S. aureus, and Gram-negative bacilli. Infection can occur either hematogenously or by direct contamination during catheter placement. Risk factors include immunocompromised states and PUPPP, as with the case of this patient.
| Introduction |
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| Caser report |
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Physical exam revealed an elevated blood pressure (160/90 mmHg), and a diffuse papular rash with several excoriated areas on the forearms. Her lower back, however, was free of lesions. Laboratory values revealed hemoconcentration and leukocytosis (Table
). Uric acid was 6.6 mg·dL1; with transaminases and bilirubin values being normal. A 24-hr urine collection yielded 8 g protein.
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One week after discharge, the patient experienced increasing back pain radiating to her right leg. She was afebrile, and otherwise asymptomatic. Physical examination revealed a slightly tender 1 cm nodule without erythema or drainage at the previous epidural catheter site. Motor and sensory examinations were normal, and the patient was advised to take analgesics and return if symptoms worsened. She returned within 24 hr. Examination at this time revealed decreased sensation to light touch over the right thigh in the L3-4 dermatome distribution. Relevant laboratory values included a white blood cell count of 17,800·mm3, platelet count of 486,000·mm3, C-reactive protein of 8.8 mg·dL1, and erythrocyte sedimentation rate = 50 mm·hr1 all consistent with a pronounced inflammatory response. Blood cultures drawn at that time grew coagulase-negative Staphylococcus in one out of four bottles. The magnetic resonance imaging (MRI) demonstrated a collection of fluid posterior to the spinal canal at the L3-4 level causing minimal cord compression (Figure
). The patient was re-admitted and, after consultation with the on-call neurosurgeon, underwent an emergency decompressive laminectomy. Wound cultures revealed methicillin-sensitive Staphylococcus aureus. The patients pain improved and she was discharged on the third post-operative day with a six-week course of iv ceftriaxone. The patient remained well, and by six weeks post-partum, her laboratory values showed no further evidence of infection or inflammation (Table
).
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| Discussion |
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An abscess will usually extend three to five segments, but can be more extensive. The most common organisms are coagulase-negative Staphylococci, S. aureus, and Gram-negative bacilli.2 The mechanism of infection can be either hematogenous seeding or direct contamination from catheter placement. The risk is higher with longer (> three days) duration, diabetes or other immunocompromised states, and low molecular weight heparin prophylaxis.1 Additionally, it has been suggested that skin abnormalities may also increase the risk of EA.5
Pruritic urticarial papules and plaques of pregnancy is an ill-defined cutaneous eruption of pruritic lesions, most commonly occurring in primigravidas in the third trimester.6 It is the most common dermatosis of pregnancy occurring in about 0.5% of pregnancies.7 The lesions are typically found on the lower abdomen and proximal extremities, and typically spare the face, palms, and soles of affected individuals.6 Treatment is symptomatic, with topical corticosteroids and diphen-hydramine as first-line therapy.8 Systemic corticosteroids are typically used in refractory cases.7 In this case, the patient was in great distress and steroids were started immediately after diagnosis.
Clearly, this patients EA most likely occurred as a result of labour epidural placement, since both the catheter placement and the EA occurred at the L3-4 level. Whether her infection resulted from direct seeding or hematogenous spread is unknown. Of course, even with strict aseptic technique, some amount of contamination with skin flora may be introduced with the epidural needle.9 However, as she had a diffusely pruritic rash with several excoriated areas, it is also reasonable to hypothesize that scratching could have resulted in colonization of lesions and transient bacteremia. Microtrauma to epidural vessels occurring with epidural placement or removal during a bacteremic period could then result in seeding of the epidural space. Whether such patients should receive antibiotic prophylaxis or even be denied epidural analgesia is unclear. Clinical judgment should be individualized to each circumstance. In either case, this patients immunosuppression from steroids placed her at higher risk for development of an epidural abscess and likely masked the resulting inflammatory reaction (e.g., lack of fever or erythema). In the face of immunosuppressive drugs, it is especially critical that the clinician be suspicious of new back or radicular pain.
Another issue raised by this case is how to minimize the risk of contamination or colonization of the catheter, epidural skin site, or epidural space through either chemical or physical means. One method is to optimize the choice of skin preparation solution. Traditional practice dictates the use of an iodophor such as povidone-iodine. While it is an effective antimicrobial agent, proper use requires allowing sufficient time for the solution to dry. In recent years, chlorhexidine gluconate (CHG) emerged as the skin preparation of choice for central venous access, given a number of studies showing lower rates of catheter-associated bloodstream infection.10 Such a change has not occurred with epidural catheter insertion. The package insert for ChloraPrep® (2% CHG in 70% isopropyl alcohol, Medi-Flex, Inc., Leawood, KS, USA) specifically cautions against use of the product for lumbar puncture, due to a lack of supporting studies at the time of FDA approval (personal communication, Medi-Flex, Inc.). More recent studies have either shown a reduction11 or no change12 in the rate of epidural catheter colonization, although the studies used 0.5% chlorhexidine vs the 2% formulation which is marketed currently. This concentration difference may prove relevant to both concerns of efficacy and possible toxicity of CHG. There are only limited clinical data regarding the neurotoxicity of CHG. Two animal studies demonstrated both ototoxicity13 and ocular toxicity14 when applied directly to the target organs. No study, however, has addressed the potential toxicity of CHG used for skin preparation prior to neuraxial procedures. Another skin disinfectant studied for this purpose is DuraPrep® (3M Health Care, St. Paul, MN, USA), a solution of an iodophor in 74% isopropyl alcohol. A recent study15 demonstrated a lower number of positive skin cultures both immediately and at catheter removal when using DuraPrep, suggesting both increased initial bactericidal activity and prolonged action. Taken together, the above results indicate that plain povidone-iodine may not be the best antiseptic for neuraxial procedures.
In addition, the use of barriers for asepsis is equally important. In North America, the generally accepted practice includes wearing a surgical cap, mask, and sterile gloves. In the United Kingdom, however, it is common to also wear a sterile surgical gown. This potentially would avoid the risk of the catheter brushing against the nonsterile arm of the anesthesiologist. Finally, use of bacterial filters for both bolus dosing and maintenance infusions may prevent seeding of the catheter and/or epidural space with pathogenic organisms arising from contaminated syringes or solutions.16
In conclusion, a parturient developed an EA despite strict adherence to a standard protocol involving appropriate skin preparation, accepted aseptic technique (mask, cap, sterile gloves), and use of a bacterial filter. The placement of the epidural was notably atraumatic. As this was the first EA experienced in a large volume practice (3,0004,000 deliveries per year), it is our view that patient factors rather than performance factors best explain this occurrence. The predisposing patient factors included the relative immunosuppression induced by steroid therapy, and the extensive excoriations secondary to scratching of her pruritic urticarial papules and plaques of pregnancy. Microtrauma to epidural vessels during either catheter insertion or removal likely resulted in seeding of the epidural space by a common skin pathogen (S. aureus) previously introduced into the circulation through the excoriations. Consequently, donning a sterile gown would have not provided additional protection for this patient, although it certainly would not have been an unreasonable thing to do. Prophylactic antibiotics to cover skin flora (e.g., cefazolin) could have been considered, but would have exposed the fetus to antibiotics potentially complicating any neonatal sepsis evaluation. Steroid-induced immunosuppression was a likely contributing factor in the development of a full-blown infection and delayed its recognition. In immunocompromised patients, therefore, a meticulous sterile technique should be used and a high index of suspicion is warranted, as classic signs and symptoms of an epidural abscess may be masked.
| Footnotes |
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Competing interests: None declared.
| References |
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