Flaccid paralysis following subarachnoid block: A diagnostic dilemma.

INTRODUCTION

Neurologic injuries secondary to central neuraxial block are extremely rare.[1] Aetiology could be traumatic or non-traumatic. The anatomical site of damage could be the spinal cord, nerve roots or spinal vasculature. Mechanical, ischaemic, and neurotoxic insults have an additional contributory effect.[2] We present a case of acute onset paraplegia following a subarachnoid block in an elderly female and discuss the aetiology, differential diagnosis, prognosis and treatment.

CASE REPORT

An 85-year-old female with fracture neck of femur and no other co-morbidity was scheduled for a cemented hemi-arthroplasty. Her height was 4 feet and 5 inches, and her weight was 35 kg. Her baseline investigations were normal, but examination of the spine revealed dorso lumbar kyphoscoliosis.

Standard monitors were attached including electrocardiogram, pulse oximetry and non-invasive blood pressure. Combined spinal epidural anaesthesia was planned but difficulty was anticipated due to the spinal deformity. An 18 gauge Tuohy needle was inserted in the midline at L3 -L4 intervertebral space with the patient in the sitting position. Technique used was loss of resistance to air but this could not be appreciated by the anaesthesiologist and dural puncture occurred during third attempt; in the first two attempts, the needle was hitting the lamina of the spinous processes. A volume of 1.8 mL 0.5% hyperbaric bupivacaine along with 25 μg fentanyl was administered intrathecally. A level of the block till T10 was achieved; intraoperative vitals were stable. Duration of surgery was 2 h. Fluids administered included the maintenance volume calculatetd by 4:2:1 rule and additional 1 L of crystalloids, followed by 2 L in the next 24 h. She was monitored for post-dural puncture headache for the next 48 h. The post-operative pain was managed by tramadol. She developed fever 9 h after surgery. She also complained of tingling and weakness in both lower limbs. She was restless and anxious during the neurological examination. There was absence of deep tendon reflexes (plantar, ankle and knee), muscle weakness (Grade 1/5 for flexors and extensors of hip and knee), decreased tone and absent sensation to pain, touch and vibration in bilateral lower limbs and a diagnosis of a lower motor neuron type of paralysis with sensory involvement was established. The neurological examination was repeated after 12, 24 and 48 h. By the 2nd day, there was some improvement in motor power (Grade 2/5 for flexors and extensors of hip and knee). There was no bladder or bowel involvement (assessed on day 1 and day 2).

Magnetic resonance imaging (MRI) of the dorsolumbar spine after 24 h revealed spondylodiscal degenerative changes with diffuse disc bulge causing thecal sac compression and bilateral foraminal nerve root compression at L1 -L2, L2 -L3, L3 -L4 and L4 -L5 levels along with bilateral lateral recess stenosis at L1 -L2 and L2 -L3 levels and mild canal stenosis at L1 -L2 and L2 -L3 levels. Spondylolisthesis of C4 over C5 with diffuse disc bulge from C3 to C7 levels was also noted.

The patient was managed conservatively. There no history of infection, fever or previous neurological complaint in the lower limbs in the previous 2–3 months preceding this surgery from the patient and the relatives (primary care providers for the patient). Nerve conduction study (NCS) was done on the 3rd day which reported demyelinating, axonal mixed sensory-motor polyneuropathy. Cerebrospinal fluid (CSF) analysis did not report any abnormality. A presumptive diagnosis of Guillain–Barre syndrome (GBS) was made. Intravenous immuno globulin was not administered as the neurologic impairment (motor and sensory deficit) was non-progressive. She started to show neurologic recovery by the 4th day with grade of the muscle power of 3/5 (flexors and extensors of hip and knee) and 50% sensory loss. She was discharged from the hospital after 10 days with no sensory impairment and a muscle power of 5/5 (flexors and extensors of hip and knee). She recovered completely in 2 months.

DISCUSSION

Regression of sensory and motor blockade after neuraxial anaesthesia should be monitored as the “sixth vital sign.” Risk factors for development of perioperative nerve injury are pre-existing neurologic disorders, diabetes mellitus, extremes of body habitus, male gender, advanced age, direct surgical trauma, compressive dressings, tourniquet inflation, haematoma, abscess and improper patient positioning.

Direct trauma to the spinal cord and the nerve roots during insertion of spinal or epidural needles and catheters is characterized by unilateral limb paralysis, numbness, weakness, and pain.[2] Non-traumatic causes range from vascular, inflammatory, toxic and allergic disorders to acute polyradiculitis, GBS, hyperkalaemic or hypokalaemic paralyses.[1] MRI is the gold standard for diagnosing compressive lesions. Immediate decompression is warranted; likelihood of full or partial recovery is good if it is managed within 8 h.[3]

Acute transverse myelitis is a demyelinating lesion characterised by upper and lower motor neuron signs. It has been reported immediately, 2 days and 2 weeks after uncomplicated central neuraxial block.[456] Cauda equina syndrome is characterised by weakness and sensory loss of bilateral lower limbs, buttocks, perineum and bladder, bowel and sexual dysfunction. Reduced amplitudes of compound motor action potentials and neurogenic changes in the supplied muscles are confirmatory.[7] GBS is characterised by ascending flaccid paresis and loss of reflexes, which follows 1–4 weeks after an infection.[8] The clinical presentation in our patient was atypical, but the diagnosis was established on the basis of NCS. Albumino-cytological dissociation is seen in the CSF, but it can be normal during early stages (up to 1-week). Development of GBS in our patient was a co-incidental association.

Some authors have reported development of GBS after epidural anaesthesia.[910] Interaction between the local anaesthetic agents and myelin sheaths or local trauma to nerve roots could be a precipitating event. American Society of Regional Anaesthesia and Pain Medicine does not preclude administration of regional anaesthesia in patients with the pre-existing neurologic disease.[3]

CONCLUSION

Any delay in recovery after spinal anaesthesia should be thoroughly investigated. First and foremost in such a scenario is to make an attempt to diagnose or exclude a medical or surgical emergency. A definitive diagnosis may be difficult to establish in some cases and management should then be based in accordance with the few differentials. Development of GBS in the immediate perioperative period led to the diagnostic dilemma, but a methodological and sequential evaluation of the patient enabled us to establish the diagnosis and initiate treatment.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.