Rapid postoperative onset of neurological dysfunction.

A 69-year-old woman with severe rheumatoid arthritis was admitted with rigors 3 weeks following a left total knee replacement. She had a severe deforming arthropathy with an unstable cervi-cal spine and had had multiple joint replacements. She was being treated with prednisolone and penicillamine. The left knee was slightly warm but there was no effusion or restriction of movement. There were no signs of meningitis. She had a superficial pressure sore over the 8th thoracic vertebra. Urinalysis showed proteinuria and she had a leucocytosis. She was treated with co-amoxiclav (625 mg 8 hourly, oral) for suspected urinary tract infection and flucloxacillin (500 mg 6 hourly, oral) for possible staphylococcal septicaemia in view of the pressure sore and recent joint replacement. Urine and blood cultures were subsequently negative. Her condition deteriorated over the next day and her antibiotic regimen was changed to cefotaxime (1 g 8 hourly, intravenously) and vancomycin (1 g 12 hourly, intravenously) as empirical treatment of septicaemia of undetermined origin. She responded well, but four days later she dislocated her right total hip replacement whilst turning over in bed (an event which had happened twice previously). The hip was relocated under spinal anaesthetic using marcaine in dextrose. Initially the anaesthetist aspirated clear cerebrospinal fluid (CSF) but aspiration following introduction of marcaine revealed purulent CSF. Examination of the CSF revealed 40 red blood cells/mm3, 2920 white blood cells/ mm3 (98% neutrophils) and Gram-positive cocci were seen on microscopy. A few hours postoperatively she became unrousable and had developed neck stiffness. Neurological examination at this time was very difficult in view of her condition, though her left plantar reflex was equivocal. However, because of the paucity of neurological signs, the neuro-radiologists felt that magnetic resonance imaging (MRI) was not indicated. Within a week, her ankle, knee and plantar responses became absent. Sensory examination remained difficult to interpret because of poor cooperation but it was felt that there was abnormal sensation from L4 down. Questions 1 What is the diagnosis? 2 What other conditions are in the differential diagnosis? 3 What is the treatment of choice for this patient? 261