Although extremely rare, neurological lesions following spinal or epidural anaesthesia are the most feared complications because they can lead to mechanical or chemical impairment of the spinal cord or its coverings. In most cases, the symptoms subside after a time and disappear . Occasionally, however, neurological complaints after regional anaesthesia can be symptoms of an early pre-existing disease which would be diagnosed in due course .
We report the case of a 77-year-old patient who complained of paraesthesia, loss of sensitivity and pain in her legs after a spinal puncture.
A 77-year-old female patient underwent a curettage because of postmenopausal bleeding; the patient requested spinal anaesthesia.
We used a 22-gauge Quinke needle for the puncture and injected 2 mL hyperbaric mepivacaine 4% as local anaesthetic. Although the patient's anatomy appeared normal under palpation, the puncture was extraordinarily difficult. After several unsuccessful attempts at different levels, success was achieved, without causing any paraesthesiae, via medial access at L2-L3. Injections at higher levels should be avoided because of the increased risk of injuring the spinal cord. Even under specific questioning, during the initial attempts, the patient did not report any abnormal sensations. Despite the demonstrably intrathecal placement of the needle, clear cerebrospinal fluid (CSF) before injection, there was no anaesthesia even 15 min following the injection of mepivacaine. The absence of spinal anaesthesia was attributed to an inadvertent change in the position of the needle during injection of the anaesthetic of the needle; therefore, general anaesthesia was induced. The patient left the recovery room without any neurological symptoms after one hour of post-operative observation.
Several days later, she was scheduled for total hysterectomy for a corpus carcinoma. During the preanaesthetic visit, the patient complained that paraesthesia in her legs, more right than left, had started immediately after the unsuccessful spinal anaesthesia. She also stated that the problems were already decreasing. The hysterectomy was performed under general anaesthesia and the patient left the hospital several days later.
Because of the persistence of the neurological symptoms, the patient came back one week later for a neurological examination. In addition to clinical examination, functional diagnostic examinations including EMG, EEG, sensory evoked potentials and nerve conduction measurement were performed. The findings were either normal or age-related, but unrelated to the symptoms. Radiological imaging did not reveal anything remarkable in the spinal column. The patient refused myelography, because she feared another spinal puncture, so examination of CSF was not possible. Skeletal scintigraphy indicated no pathological activity. Sonography did not show reduced blood flow in the lower extremities. General findings included a nodal struma with an autonomic adenoma and eczema of the legs caused by chronic venous insufficiency. The ECG showed a left ventricular hypertrophy. However, the NMR imaging showed syringomyelia from T6 to T10 as the pathological cause of her complaints.
Although several attempts were made to obtain further information, in view of the state of health of the patient, we were unsuccessful in getting any further data.
In the presence of persisting neurological symptoms after spinal or epidural anaesthesia, one should always consider not only an iatrogenic lesion, but also the exacerbation of a pre-existing disease with no relation to the anaesthetic procedure.
In the present case, we first suspected an iatrogenic lesion because the symptoms began soon after spinal puncture and injection of the anaesthetic. We considered direct and an indirect traumatic lesion of the spinal cord in the area of the injection, although this was unlikely because of the extension of the symptoms to L4-L5. We also considered peripheral nerve lesions or metastases of the primary tumour in the lumbar segments. Only the NMR imaging of the thoracic segments showed a syringomyelia. Neurosurgical intervention was not indicated at this time.
The pathogenesis of syringomyelia is still unclear. Usually, the symptoms of the disease increase slowly, and may remain stable for years. An increase in the cystic cavities in the spinal cord and increased pressure in the cavities causes the symptoms [3,4]. Some patients develop a severe kyphoscoliosis as a result of muscular atrophy .
However, in some cases, a sudden onset is possible [6,7]. The trigger may be a sudden, direct increase in pressure within the cystic formations. In the present case, an indirect increase may have been responsible. Because of the loss of CSF, a craniospinal pressure dissociation occurred. If we assume a valve mechanism between the central canal and the syringe cavity, CSF could have been sucked into this cavity. Changes in the lumbar pressure are transmitted to the fluid in the cavity and cause a higher pressure than in the surrounding structures [8,9].
Because of the atypical symptomatic manifestation of this case, only systematic neurological examination and NMR imaging were able to provide a diagnosis.
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