Neurological complications of lumbar epidural anesthesia and analgesia.

      Neurological complications of lumbar epidural anesthesia and analgesia.

                                     Dr KS Dhillon

Introduction

Epidural anesthesia and analgesia (EAA) are widely used in clinical practice for surgery and postoperative analgesia. Epidural anesthesia and analgesia reduces or eliminates perioperative physiological stress responses to surgery and this inturn decreases surgical complications and improve clinical outcomes[1-3].

Studies have shown a significant reduction in perioperative cardiac morbidity, pulmonary infections, deep vein thrombosis, pulmonary embolism, ileus, acute renal failure, blood loss and need for transfusion. The length of hospital stay and the 30 day mortality is also reduced with EAA [4]. EAA is also believed to preserve postoperative immune function by attenuating the stress response of surgery. Studies have shown significant reductions in the incidence of postoperative infections in patients treated with EAA [5,6].

EAA is generally regarded as safe and effective but EAA can be associated with serious complications. Though the complications are rare they can sometimes be devastating.

Neurological complications of lumbar epidural anesthesia and analgesia.

Studies show that the frequency of severe, permanent neurological complications related to epidural catheterisation is low at about  0.1–1/10,000 procedures [7-12]. Epidural anesthesia can be associated with radiculopathy, cauda equina syndrome and myelopathy leading to permanent neurological disability [13]. Compression of the spinal cord or nerve roots can occur from extradural abscesses or haematomas. Arterial and venous infarction of the spinal cord and nerve root trauma can occur during catheter placement. Chemically induced arachnoiditis by the drugs used for the epidural has also been implicated in causing permanent neurological disability [14-18].

Lumbar epidural injections in patients with pre-existing spinal stenosis can  precipitate severe and widespread lumbosacral polyradiculopathy [13,19].

Neurotoxicity from local anesthetics is a well known phenomenon and is related to the type and concentration of anesthetic and its systemic absorption. Intrathecal lignocaine at high doses has been associated with neurologic side effects [20,21].

Epidural catheters can inadvertently penetrate the dural space, cause damage to neurovascular structures and also can lead to infection. The incidence of accidental dural puncture during needle insertion is about 0.16–1.3% and the incidence of postdural headache in these patients is about 16–86% [22-25].

Nerve root irritation by the catheter and intrathecal injection of local anesthesia can produce transient neurologic symptoms (TNS) such as  sharp radicular back pain and paresthesias [26].

Risk factors for TNS include the use of lidocaine as the local anesthetic, lithotomy position, obesity, and performance of the procedure in the outpatient department [27].The TNS usually usually resolve once the catheter is removed. Epidural abscesses and meningitis following epidural and spinal anesthesia is rare [28].

Risk factors for meningitis include dural puncture, non sterile technique, prolonged indwelling catheter and septicemia [29,30]. Paraplegia, the most serious complication of epidural anesthesia can be caused by an epidural hematoma which forms during catheter placement or removal. The secondary cause of this complication is the concomitant pre-, intra-, or postoperative administration of drugs that affect blood coagulation (anticoagulants) [31].  Spinal abscesses and anterior spinal artery syndrome are also known to cause paraplegia. Epidural haematoma formation is a rare complication with an incidence of less than 1 in 150,000 [32].

Injury to the spinal vasculature during catheter placement has been described and the incidence is about 3–12%. Despite injury to spinal vasculature symptomatic epidural hematomas are rare [33,34]. Early recognition of symptomatic epidural haematomas and decompressive laminectomy within 8 hours have been shown to improve clinical outcomes [35].

Epidural abscess and meningitis

The reported incidence of epidural abscess after epidural catheterisation is about 1 : 1000 and for meningitis is about 1 : 50 000 [36].

There are several ways in which bacteria may enter the epidural space. One of the sources of infection is needle or catheter contamination and lack of barrier precautions, such as the use of chlorhexidine 0.5% in 70% alcohol for skin disinfection [37-39]. Contamination of the needle or catheter by oropharyngeal and nasal flora of the anesthetist has been proven by cultures obtained from the epidural abscess and from the anaesthetist [40,41].

Epidural solution can be a source of epidural infection despite the use of bacterial filter. There is some evidence to suggest that frequent syringe changes could be associated with a higher rate of epidural infection  [42-44]. The 500-ml bags of epidural infusion fluid has not been found to be  associated with epidural abscesses or meningitis [45].

Infection of the insertion site of the catheter with migration of the bacteria along the catheter tract is a common mechanism of epidural infections. A haematogenous source of epidural infection after epidural catheterisation is uncommon [46-48].

There are several predisposing factors for epidural infection. Patients who are immunocompromised are more likely to develop infection [49-51]. Difficulty in insertion of epidural catheter is also a known risk factor for infection. Difficulty in insertion is associated with the formation of asymptomatic epidural haematoma [49,52,53] or subcutaneous haematoma which can act as a nidus for infection [54]. Epidural analgesia of more then 3 days is associated with higher infection rates [51].

Staphylococcus is the most common organism cultured from epidural abscesses [49,50,51,55]. Methicillin resistant staphylococcus has also been cultured in some of these abscesses.

Patients with an epidural abscess usually presents with midline back pain and fever about 5 days after epidural insertion [49-51]. If untreated neurological deficit with paraplegia usually develops within a week [49]. The prognosis for recovery is poor once paraplegia develops [49,56].
Meningitis usually results from dural puncture and patients present with headache and fever, with some patients developing neck rigidity [50]. In some patients who developed meningitis there were no reports of dural puncture [45].

In patients suspected to have an epidural abscess, an MRI scan is the investigation of choice [58]. Sometimes back pain is ascribed to musculoskeletal pain and a delay in diagnosis can result. Therefore a high index of suspicion is necessary to prevent delays in diagnosis.

A lumbar puncture with csf microscopy is necessary for the diagnosis of meningitis [45].
Epidural abscesses are treated with a combination of early surgical decompression and prolonged antibiotic therapy [53]. Patients with minimal or no neurological deficit can be managed with antibiotics alone [55].

Epidural haematoma

Coagulopathies predispose patients to epidural haematomas following epidural catheter insertion [56]. Hence the timing of anticoagulant administration is important in reducing the risk of epidural haematomas [59,60]. The newer recommendations, recommend that low molecular weight heparin administration for prevention of deep vein thrombosis (DVT) be delayed for 24 h in case of a bloody tap [60]. Another risk factor for the development of epidural haematoma is difficulty in identifying the epidural space [61].

Difficulty in identification of the epidural space can often be encountered in patients who are obese. Other risk factors include advanced age, female gender and bony spinal pathology [50].
The usual clinical presentation of an epidural haematoma is radicular back pain with rapidly progressive neurological (motor and sensory) deficit and sphincter dysfunction [56]. The symptoms usually develop within 24 hours of either epidural insertion or removal, but sometimes the onset of symptoms may be delayed [50].

An MRI scan of the spine is the investigation of choice in patients suspected of having an epidural haematoma. Often the neurological deficit is attributed to the epidural infusion and the back pain to a musculoskeletal cause and this leads to a delay in diagnosis [62]. Early diagnosis is of paramount importance since a favourable outcome is dependent on early spinal decompression within 8 hours of the onset of symptoms [56]. Neurological outcome depends on the extent of the neurological deficit, the size of the haematoma and the time between haematoma formation and surgical decompression [56].

Leg strength monitoring is essential in assessment of spinal cord health
in patients receiving epidural analgesia [41]. The Bromage scale is commonly used to measure motor block [63].

Grade Criteria                                                                  Degree of block

I          Free movement of legs and feet                            Nil (0%)

II        Just able to flex knees with free movement
           of feet                                                                   Partial (33%)

III       Unable to flex knees, but with free movement     Almost complete
          of feet                                                                    (66%)

IV        Unable to move legs and feet                             Complete (100%)   


Table 1. Bromage scale

The perfect analgesic technique would provide complete pain relief with no motor block. Leg weakness during epidural analgesia must be treated with suspicion until proven to be reversible. [42].  Patients who have significant weakness of the leg should have epidural infusion stopped and if no motor recovery occurs within 4 hours, an urgent MRI scan should be performed [45] .

Direct penetration of the spinal cord during epidural catheterisation and subsequent injection of fluid into the substance of the cord, leading to localised hydromyelia has been proposed as one of the mechanisms for severe neurological complications resulting from epidural anaesthesia and analgesia [64]. Examination shows segmental levels of motor and sensory impairment which corresponds to the level of spinal cord injury. MRI shows tubular, clearly demarcated lesions which are hyperintense on T2 weighted images and hypointense on T1.

Air bubbles in the cord has been identified in patients who have become paraplegic after epidural anesthesia [65].

Local anesthetic drugs have been found to be potentially neurotoxic in experimental studies [66]. Polyethylene glycol found in methylprednisolone acetate is known to cause necrosis of neuronal tissue [67]. Injection of these neurotoxic drugs into the cord can cause damage to the cord.
Intravenous high dose methylprednisolone may be of value in these patients with cord damage.

Arachnoiditis and subarachnoid cyst

Arachnoiditis as a complication of epidural anesthesia has been reported.  Torres et al [68] reported 7 cases where patients developed arachnoiditis following epidural anesthesia. Subarachnoid cysts developed in all patients and in 5 cord cavitation developed. MRI was found to be useful in the detection of the arachnoiditis and the intramedullary cysts, as well as to monitor the extent of the lesion and progression of the lesions. In one case a tethered cord was present and in another there was spinal cord atrophy.

Possible etiology of these complications include scars from meningeal inflammation which induce ischemia leading to cavitation. CSF circulation blockade can also cause dilation of the central spinal canal which results in ischemia from compression followed by myelomalacia and cavitation.
Although progressive inflammation of the arachnoid due to trauma, infection, or hydrocortisone has been reported since the early 1970s,  coexistence of extensive syringomyelia (ES) and a giant anterior arachnoid spinal cyst (AASC) had not been reported until 2012. In 2012 Hirai et al [69] reported a case of adhesive arachnoiditis with extensive syringomyelia and a giant arachnoid cyst after spinal and epidural anesthesia. They had a  29 years old woman who presented with sudden anuresis 5 months after spinal/epidural anesthesia for cesarean section. She subsequently developed paraplegia with numbness below the chest. An MRI showed a giant AASC compressing the spinal cord at T1-T6 and there was an adhesive lesion at T7. Slight improvement in motor function occurred after
posterior laminectomy at T6-T7 and adhesiolysis at T7. Three years after the surgery motor function deteriorated further and posterior laminectomy at T5-T6 with insertion of a cyst-peritoneal shunt into the AASC was carried out.

Nogués et al [70] published a report where 3 women who had epidural anesthesia for gynecological surgery developed spinal arachnoiditis which led to subarachnoid cysts and cord cavitation. They found that MRI is useful for making a diagnosis and monitoring the extent and progress of the lesion.

Conclusion

Epidural anesthesia and analgesia (EAA) are extensively used in clinical practice for surgery and postoperative analgesia. Epidural anesthesia and analgesia reduces surgical complications and improve clinical outcomes.

Studies show a significant reduction in perioperative cardiac morbidity, pulmonary infections, deep vein thrombosis, pulmonary embolism, ileus, acute renal failure, blood loss and need for transfusion with EAA. The length of hospital stay and the 30 day mortality is also reduced with EAA. The incidence of postoperative infections is significantly reduced in patients treated with EAA. Though EAA is generally regarded as safe and effective, serious devastating neurological complications can occur following EAA.

Epidural abscess, meningitis, epidural haematomas, hydromyelia, cord cavitation, arachnoiditis and arachnoid spinal cysts are known complications of EAA which can produce serious and sometimes permanent neurological deficit including paraplegia. Prompt diagnosis and early aggressive treatment is essential for a good clinical outcome.

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