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A 34-year-old male was admitted for cystolithotripsy. He was a diagnosed case of Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) and at admission, gave history of 'cold attacks' over knee joints, numbness over right lower limb and intermittent sweating all over the body. History revealed that patient had difficulty in urination followed by retention, over one year ago and was managed conservatively with bladder catheterisation and medications. He had developed tingling over the sole of both feet and later over the legs which extended towards gluteal region as well. He had difficulty in walking and developed giddiness and blurring of vision. There was blunting of sensation in legs with a patchy distribution. There were no cranial nerve palsies, disturbed deep tendon reflexes or ophthalmic demyelinating signs.Visual evoked potential study was insignificant. Dermatologist opinion was sought and it was in favour of the diagnosis of demyelinating polyneuropathy. Magnetic Resonance Imaging (MRI) plain and with contrast had revealed acute demyelination of lumbar spinal cord and cerebral cortex. Patient was also found to have hypovitaminosis D3. Diabetes mellitus, trauma and viral infections were ruled out. Serum electrolytes, autoimmune antibody levels and tumour necrosis factor levels were normal. Patient was managed with rest, steroids, antibiotics, multivitamins (including vitamin D) and lorazepam. Follow-up MRI brain and spine 3 months later showed complete resolution of previous brain lesions but new scattered bifrontal subcortical white matter lesions, with L4-L5 and L5-S1 mid posterior disc bulge. He was subsequently put on oral gabapentin, pregabalin, baclofen, acetaminophen. At discharge, patient had persistent, minimal paraesthesia over right lower leg and on lower back and was off catheter.At the time of present admission, the investigation reports were normal and patient had been only on oral gabapentin and vitamin D supplements. Patient was on urinary catheterisation for two days and preoperative antibiotics. Subarachnoid block was planned and informed written consent was obtained. Routine nil per oral precautions were taken and patient was preloaded with Ringer lactate (500 ml) IV before shifting to operation theatre. Routine monitors were connected. Basal blood pressure (BP) was 130/90 mm Hg and pulse rate (PR) 66 per min. Patient was administered subarachnoid block (SAB) with bupivacaine 0.5% heavy, 7.5 mg (1.5 cc) with 10 μg of dexmedetomidine (0.5 cc volume) (Dextomid®, Neon Laboratories, India, 50 μg / 0.5 cc ampoule, diluted to 2.5 cc with normal saline)(total 2 ml volume)in supine left lateral position at L4-L5 interspace.The sensory block at 5 th min reached T12 dermatomal level and at 10 th min, to T8 level. Motor blockade reached Bromage scale grade IV by 5 th min. Patient developed 4 episodes of hypotension (fall of systolic BP>25% from basal) in first 30 min and was managed with mephentermine (45 mg in total) and increased rate of infusion of Ringer lactate (RL). Pulse rate varied fro...
A 34-year-old male was admitted for cystolithotripsy. He was a diagnosed case of Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) and at admission, gave history of 'cold attacks' over knee joints, numbness over right lower limb and intermittent sweating all over the body. History revealed that patient had difficulty in urination followed by retention, over one year ago and was managed conservatively with bladder catheterisation and medications. He had developed tingling over the sole of both feet and later over the legs which extended towards gluteal region as well. He had difficulty in walking and developed giddiness and blurring of vision. There was blunting of sensation in legs with a patchy distribution. There were no cranial nerve palsies, disturbed deep tendon reflexes or ophthalmic demyelinating signs.Visual evoked potential study was insignificant. Dermatologist opinion was sought and it was in favour of the diagnosis of demyelinating polyneuropathy. Magnetic Resonance Imaging (MRI) plain and with contrast had revealed acute demyelination of lumbar spinal cord and cerebral cortex. Patient was also found to have hypovitaminosis D3. Diabetes mellitus, trauma and viral infections were ruled out. Serum electrolytes, autoimmune antibody levels and tumour necrosis factor levels were normal. Patient was managed with rest, steroids, antibiotics, multivitamins (including vitamin D) and lorazepam. Follow-up MRI brain and spine 3 months later showed complete resolution of previous brain lesions but new scattered bifrontal subcortical white matter lesions, with L4-L5 and L5-S1 mid posterior disc bulge. He was subsequently put on oral gabapentin, pregabalin, baclofen, acetaminophen. At discharge, patient had persistent, minimal paraesthesia over right lower leg and on lower back and was off catheter.At the time of present admission, the investigation reports were normal and patient had been only on oral gabapentin and vitamin D supplements. Patient was on urinary catheterisation for two days and preoperative antibiotics. Subarachnoid block was planned and informed written consent was obtained. Routine nil per oral precautions were taken and patient was preloaded with Ringer lactate (500 ml) IV before shifting to operation theatre. Routine monitors were connected. Basal blood pressure (BP) was 130/90 mm Hg and pulse rate (PR) 66 per min. Patient was administered subarachnoid block (SAB) with bupivacaine 0.5% heavy, 7.5 mg (1.5 cc) with 10 μg of dexmedetomidine (0.5 cc volume) (Dextomid®, Neon Laboratories, India, 50 μg / 0.5 cc ampoule, diluted to 2.5 cc with normal saline)(total 2 ml volume)in supine left lateral position at L4-L5 interspace.The sensory block at 5 th min reached T12 dermatomal level and at 10 th min, to T8 level. Motor blockade reached Bromage scale grade IV by 5 th min. Patient developed 4 episodes of hypotension (fall of systolic BP>25% from basal) in first 30 min and was managed with mephentermine (45 mg in total) and increased rate of infusion of Ringer lactate (RL). Pulse rate varied fro...
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