The present study demonstrated spinal surgery to be the cause of the cauda equina lesions in about 15% of patients. In our population cauda equina lesions occurred during lumbar disc and spinal stenosis surgery. During study period such lesions occurred in 0‰, 1.5‰, and 6.6‰ of spinal surgeries performed in neurosurgical, major orthopaedic, and regional hospital departments in Slovenia, respectively. Neurogenic lesions in these patients were demonstrated by objective methods of clinical neurophysiology in addition to clinical examination (Tables , ). Clinically, all patients, but one (# 11) had clearly impaired touch and pinprick saddle sensation (Table ). On EMG of the EAS muscles in 5 patients spontaneous denervation activity and in another 3 MUPs reinnervation changes were found. These electrodiagnostic abnormalities pointing to sacral root lesions were substantiated by pathologic measurements of the penilo-/clitoro-cavernosus reflex in all but 3 patients (Table ). However, as patients did not report sacral symptoms preoperatively, sacral electrodiagnostic studies were performed only after and not before spinal surgery. The development of neurologic deficits during surgical procedures was therefore reliant on a history of the onset of sacral neurologic, urinary, bowel, or sexual symptoms, and on a comparison of preoperative neurologic findings (as described in patients’ files) with neurologic findings after surgical intervention. Except one patient (# 7) with normal urinary function, all other patients reported urinary incontinence or reduced bladder emptying, and 3 of patients also reported urinary urgency. Majority reported constipation, in most associated by incontinence of faeces, or at least flatus. Most included patients also reported either severe erectile dysfunction or complete sexual abstinence (Table ).
The severity of neuropathic lesions in our patients with lesions due to spinal surgery was similar to the severity in patients with non-iatrogenic causes, with the exception of urinary symptoms, which were more severe in patients with iatrogenic lesions (Table ).
In 5 patients with iatrogenic lesions included in this series spinal surgery was performed by a single orthopaedic surgeon from a regional hospital. The cauda equina lesion occurred during lumbar disc surgery in 4 of these patients (# 1, # 2, # 3, and # 5, Tables , ), which are probably preventable. Similarly a case of lumbar discectomy with dural tear during evacuation of sequestered disc material (# 4) which was performed in another regional hospital would be probably preventable. Damage could probably also be reduced by better postoperative surveillance, and prompt re-operation in both patients (# 7 and # 9) with postoperative haematoma occurring after lumbar disc surgery. The remaining 4 cases (# 6, #8, # 10, and # 11) during surgery for spinal stenosis, in which 4 different orthopaedic surgeons were involved, would appear to be more difficult to prevent.
In a retrospective review of 2,842 discectomies, McLaren and Bailey found a stenotic spinal canal (antero-posterior diameter <13 mm) at the level of the disc protrusion in 5 out of 6 cases with consequent cauda equina lesions [7
]. In all these cases a keyhole interlaminar approach was used, which did not allow enough space for postoperative swelling. Decompressive laminectomy has been suggested for surgical management of disc protrusion superimposed on spinal stenosis. Similarly, in our series 3 out of 5 patients (# 2, # 3, and # 5) with cauda equina lesion occurring after surgery (performed by the same surgeon) for large dorsolateral lumbar disc herniation also had central spinal stenosis. There were no imaging studies available for one (# 1), and sequestered disc fragment was present in the other (# 4) of remaining two patients. According to the surgical reports, our surgeons did perform decompressive laminectomies, and none of 3,011 discectomies performed in our neurosurgical and orthopaedic centres resulted in cauda equina lesion (difference between their and our proportions was significant; Z
= 1.98, p
< 0.05). In one case, from McLaren and Bailey’s series [7
], stenosis could not be identified, and the cause of the lesion was unclear. In a similar, more recent study from Sweden, Henriques et al. [4
] also noted preexisting narrowing of the spinal canal in all 5 of their patients with this complication. They suggested venous congestion triggered by postoperative oedema as a possible mechanism for the lesion [4
The exact mechanisms for lesions in our spinal stenosis patients remain unclear. In addition to causes of the cauda equina lesions described above [4
], lesions might occur because of excessive pressure or traction exerted on the nerve tissue during surgery. This is supported by the fact that all cauda equina lesions reported in this series occurred with orthopaedic surgeons who used a Kerrison rongeur, even in patients with severe spinal stenosis. In contrast, no cases from the series occurred with surgeons, who in patients with severe spinal stenosis also had the option of using a high-speed drill, and the aid of the operative microscope. Both patients (# 10 and # 11) with postoperative appearance of cauda equina lesion operated in the orthopaedic centre had severe spinal stenosis (antero-posterior diameter <10 mm, Table ). However, the difference in proportion of cauda equina lesion after spinal surgery for spinal stenosis between neurosurgical and orthopaedic centre did not reach significance (0/810 = 0‰ vs. 2/378 = 5.3‰, Z
= 0.20, p
= >0.05). Further studies are needed to reveal the causes of cauda equina lesions during spinal stenosis surgery.
Preoperative imaging modalities varied in our series of 11 patients with cauda equina lesion occurring after spinal surgery; 3 were evaluated by myelography, 4 by CT, and remaining 4 by CT myelography. These spinal imaging modalities were standard in Slovenia during the period 1996–2004. None of these patients were imaged by MRI, as this method was not as widely available as today. Nowadays, the situation changed dramatically, and majority of spinal surgery patients are preoperatively evaluated by MRI. This change may improve results of spinal surgery by allowing the surgeon to better plan the procedure. However, particularly in difficult cases MRI is often still combined with CT myelography.
Although some surgeons frankly discussed the complication with affected patients, others from our series either skipped discussion or denied the complication altogether. Those patients who did not have the opportunity to openly discuss the complication with their surgeon seem to be particularly unhappy; some even declined any further medical assistance. None of our patients with iatrogenic lesions were offered psychological support or financial compensation, which further worsened the situation.
In conclusion, the present study demonstrated that surgery to the lumbar spine is prone to cause lesions to the cauda equina in a low percentage of patients (up to 6.6‰ in our series). Such events result in severe disability and may have medico-legal consequences. As most of these complications seem potentially preventable, further prospective studies on surgical techniques and appropriate actions after the complication are needed to reduce this neglected problem.