We describe a meningitis after a spinal anesthesia (SA). A 50-yr-old man, without particular medical history, had a repair of an uncomplicated hydrocele of the tunica vaginalis performed under SA. This patient, with good oral hygiene, was afebrile the day of surgery and had a leukocyte count of 7.1 × 109/L. In the operating room, the anesthesiologist wore a mask, a hat, a sterile gown, and gloves and used an autoclave-sterilized dressing pack and sterile disposable needles and syringes. The lumbar skin appeared normal and was prepared with 2 applications of 10% polyvidone iodine. On the first attempt, the lumbar puncture (LP) was accomplished. The cerebral spinal fluid (CSF) was clear, and 75 mg of hyperbaric lidocaine was injected, which allowed the surgical procedure without complication. No perioperative antibiotic was given. Five days later, a meningitis was suspected (headache, fever of 38.8°C, nuchal rigidity, blood leukocytosis of 17.5 × 109/L), and a LP performed: the CSF was turbid, leukocyte count of 400/mm3, the protein concentration 0.9 g/L, the glucose concentration 2.2 mM (blood concentration of 6.7 mM). The immediate Gram staining revealed no bacteria. IV amoxicillin and gentamycin were administered. On the sixth postoperative day, Streptococcus mitis was found in CSF cultures. All the results of the blood cultures were negative. The clinical progression was favorable.
S mitis is a Gram-positive cocci of the viridans streptococci (VS) group, which comprises S salivarius. The common characteristic of VS is its presence in the normal oral flora (1). S mitis may be found on the skin, also. We found only 2 cases of S mitis meningitis after SA (2,3). Other VS (4–8) and an enterococcal streptococci (9), causing meningitis, have been described after SA. VS meningitis after SA develops rapidly between 12 (5) and 16 h (2,7) with no administration of perioperative antibiotics. In our case, the onset was amazingly delayed, 5 days after the LP, without evident reason. Moreover, the use of antibiotics does not prevent meningitis (9) and contributes to a delay in the onset of meningeal symptoms (mean time 9 days) (3).
The pathogenesis of CSF infection after SA is much debated. There are two possibilities: aseptic failure with direct introduction of bacteria in the sterile CSF or presence of asymptomatic bacteremia during the LP and contamination of the subarachnoid space by microscopic bleeding caused by the insertion of the needle.
The role of bacteremia during SA is controversial. In bacteremic patients, the incidence of meningitis after diagnostic LP is not significantly different from the spontaneous rate, and the risk of developing meningitis after LP is 2.1% (10).
The origin of aseptic failure can come from inadequately sterilized equipment, from contamination of the needle, syringe, local anesthetic, or sterilized equipment, by droplets spread from oropharyngeal secretions discharged by personnel present during the puncture or from contamination of the skin in the lumbar area. In our operative room, all the personnel present wore face masks. In some case reports (5,8) the mask was not worn. If a face mask were systematically worn (by all personnel present in operating room), VS meningitis after SA would no longer occur (4,8). We used single containers of polyvidone-iodine, eliminating a possible source of infection. Polyvidone-iodine has an antimicrobial activity against Gram positive and negative bacteria, even though the persistence of Gram positive cocci is noted in 32.4% of skin fragments, despite meticulous preparation (11)! In a study (12), streptococcal species and others organisms were isolated from the LP site in patients who had bacteria isolated in CSF, but no streptococci were recovered simultaneously from the skin and CSF specimen.
In our case [and in (3)], the origin of meningitis may be the failure of aseptic techniques because the results of the blood cultures were negative, and the results of the CSF cultures were positive. Because our patient had a leucocyte count of 7.1 × 109/L the day of surgery, was afebrile at the time of SA, and had no signs of infections, and because there was a noncontaminated urological surgery for hydrocele, no hematogenous spread could have logically developed. Then, the direct introduction of bacteria in CSF is possible, especially when VS are isolated.
The therapy is urgent with curative antibiotherapy. S viridans and S mitis are susceptible to the penicillin group (3), with a low minimal inhibitory concentration and a low minimal bactericidal concentration (1). In S mitis meningitis cases after SA (2,3) and in ours, all the patients were treated with penicillin and survived. Third generation cephalosporins are also used in S salivarius cases with the same efficiency: cefotaxim (5) or ceftriaxone (7).
MD Isabelle Vincenti-Rouquette
MD Fabrice Petitjeans
MD Pierre Koulmann
MD Yvon Legulluche
MD Jean-Marie Rousseau
MD Yves Diraison
MD Louis Brinquin MD
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