Anaesthetic management in a patient with multiple sclerosis
Lata M Kulkarni, CS Sanikop, HL Shilpa, Anupama Vinayan
Department of Anaesthesiology, KLE University's, Jawaharlal Nehru Medical College & KLES Dr. Prabhakar Kore Hospital, Nehru Nagar, Belgaum, India
Multiple sclerosis (MS) is an autoimmune demyelinating disorder of the central nervous system (CNS) with genetic predisposition characterized by a wide variety of neurological impairment and symptoms due to multi-focal areas of inflammation and demyelination in brain and spinal cord. [1],[2] The treatment is symptomatic and with immunosuppressant drugs as there is no cure for MS.
Prevalence, increases with latitude, is rare in Asian countries, highest in north Scotland, northern Europe, and northern United States and in Canada. [1]
Exact prevalence in India is not available, but occasionally an anaesthesiologist may encounter a case of MS.
A boy of sixteen years who was a known case of MS for past eight years presented with fracture shaft of femur following a sudden fall while on treatment of MS following a relapse and was scheduled to undergo open reduction, internal fixation. He had history of limb weakness, relapsing--remitting type with movement-induced muscle spasms, gradually progressing in all the four limbs. During past two months there was diminution of vision in both the eyes and he was restricted to bed. Bowel and bladder function was normal. There was no history of seizures, difficulty in speech, swallowing and breathing. On examination he was moderate in built, weighed 38 kg with normal pulse, blood-pressure, respiration and temperature.
CNS examination revealed a conscious patient with normal higher functions, but mentally depressed. Speech was normal. There was loss of power in all the four limbs, 2/5 in both upper limbs and 2/5 in right lower limb (left lower limb with fracture) as per Medical Research Council (MRC) rating. Co-ordination was impaired in upper and lower limbs with marked movement-induced spasticity, hyper responsive deep reflexes and up-going Babinski. He also had optic neuritis. Gait could not be tested. His sensory system, other cranial nerves, brain-stem function appeared normal. Heart-rate response to deep breathing was normal. His other systems were normal.
Laboratory investigations (routine haematological, liver and kidney function, serum electrolytes), chest X-ray and electrocardiogram (ECG) were normal.
Magnetic resonance imaging (MRI) scan showed patchy bright signals within the cord on T 2 -weighed images from C 1 to T 10 vertebral levels suggesting demyelination. No focal lesion of brain parenchyma was seen.
He was receiving oral methotrexate and folic acid, oral baclofen and methylcobalamin for last six years. Recently, he was treated with intravenous (I.V.) methyl prednisolone during an acute attack followed by tapering dose of oral prednisolone, during last 6-8 weeks.
Anaesthetic management
The patient was classified as ASA grade III physical status, and parental informed consent was obtained.
Following preoperative counselling and night premedication with oral alprazolam 0.25 mg, next morning patient was shifted to operation theatre (OT). After I.V. access midazolam 1 mg, inj. glycopyrrolate 0.2 mg, inj. ranitidine 50 mg and inj. hydrocortisone 100 mg were administered. Monitoring included oxygen saturation (SpO 2 ), ECG, non invasive blood pressure (NIBP) and end tidal carbon dioxide (EtCO 2), core temperature from the tympanic membrane. OT temperature was maintained at 22° C. Induction was done with 2.5 mg/kg of propofol and 1.5 μg/kg of fentanyl following preoxygenation and intubated with 7.5 cuffed endotracheal tube using 20 mg of atracurium and neuromuscular monitoring (NM) with Train-of-Four (TOF) ratio. He was maintained on N 2 O in O 2 (66:33), 0.6-0.8% halothane with controlled ventilation and incremental fentanyl 20 μg along with atracurium top-ups of 10 mg using N-M monitoring. I.V. Ringer lactate about 1200 ml was infused. At the conclusion of surgery neuromuscular block was reversed with neostigmine 0.05 mg/kg and glycopyrrolate 0.4 mg satisfactorily. I.V. inj. ondancetron 4 mg was administered.
Post-operatively SpO 2 , NIBP, ECG and temperature monitoring along with O 2 supplementation by ventimask was done in the recovery room. I.V. Tramadol 2 mg/kg, six hourly was used for post-operative analgesia. There was a rise of temperature 1°C, eight hours postoperatively which was treated with I.V. Paracetamol, 10 mg/kg, and cold sponging promptly. Also there was respiratory distress after twelve hours which subsided after increasing O 2 concentration to 60%. He was discharged after 10 days. There was no neurological exacerbation of the disease.
MS occurs in genetically susceptible individuals following an environmental, viral exposure that produces activated autoreactive T cells and cytokines, disrupting the blood-brain barrier. [3],[4] The inflammatory process produces demyelination and glial scarring (sclerosis) in scattered areas of brain and spinal cord that leads to conduction blockade along the neural pathways wherein Na + channels are affected by endogenous oligopeptides resembling blockade by local anaesthetics LA. [4] This results in multiple sensory deficits, cranial nerve palsies, limb weakness, paraesthesias, cardiac dysrhythmias, autonomic dysfunction, ventilatory disturbances leading to hypoxaemia and respiratory failure.[1],[2],[3]
Clinically, there are three main type:
All the types can eventually develop into a severe progressive course, ultimately leading to fixed neurologic deficits and disability. Pregnancy is associated with improvement in symptoms and relapse can occur in early post-partum months.[2],[3]
Treatment consists of [2],[3]
Currently Schwann cell transplantation is under investigation. [2]
Lata M Kulkarni, CS Sanikop, HL Shilpa, Anupama Vinayan
Department of Anaesthesiology, KLE University's, Jawaharlal Nehru Medical College & KLES Dr. Prabhakar Kore Hospital, Nehru Nagar, Belgaum, India
 Introduction |  |
Multiple sclerosis (MS) is an autoimmune demyelinating disorder of the central nervous system (CNS) with genetic predisposition characterized by a wide variety of neurological impairment and symptoms due to multi-focal areas of inflammation and demyelination in brain and spinal cord. [1],[2] The treatment is symptomatic and with immunosuppressant drugs as there is no cure for MS.
Prevalence, increases with latitude, is rare in Asian countries, highest in north Scotland, northern Europe, and northern United States and in Canada. [1]
Exact prevalence in India is not available, but occasionally an anaesthesiologist may encounter a case of MS.
| Case Report | |
A boy of sixteen years who was a known case of MS for past eight years presented with fracture shaft of femur following a sudden fall while on treatment of MS following a relapse and was scheduled to undergo open reduction, internal fixation. He had history of limb weakness, relapsing--remitting type with movement-induced muscle spasms, gradually progressing in all the four limbs. During past two months there was diminution of vision in both the eyes and he was restricted to bed. Bowel and bladder function was normal. There was no history of seizures, difficulty in speech, swallowing and breathing. On examination he was moderate in built, weighed 38 kg with normal pulse, blood-pressure, respiration and temperature.
CNS examination revealed a conscious patient with normal higher functions, but mentally depressed. Speech was normal. There was loss of power in all the four limbs, 2/5 in both upper limbs and 2/5 in right lower limb (left lower limb with fracture) as per Medical Research Council (MRC) rating. Co-ordination was impaired in upper and lower limbs with marked movement-induced spasticity, hyper responsive deep reflexes and up-going Babinski. He also had optic neuritis. Gait could not be tested. His sensory system, other cranial nerves, brain-stem function appeared normal. Heart-rate response to deep breathing was normal. His other systems were normal.
Laboratory investigations (routine haematological, liver and kidney function, serum electrolytes), chest X-ray and electrocardiogram (ECG) were normal.
Magnetic resonance imaging (MRI) scan showed patchy bright signals within the cord on T 2 -weighed images from C 1 to T 10 vertebral levels suggesting demyelination. No focal lesion of brain parenchyma was seen.
He was receiving oral methotrexate and folic acid, oral baclofen and methylcobalamin for last six years. Recently, he was treated with intravenous (I.V.) methyl prednisolone during an acute attack followed by tapering dose of oral prednisolone, during last 6-8 weeks.
Anaesthetic management
The patient was classified as ASA grade III physical status, and parental informed consent was obtained.
Following preoperative counselling and night premedication with oral alprazolam 0.25 mg, next morning patient was shifted to operation theatre (OT). After I.V. access midazolam 1 mg, inj. glycopyrrolate 0.2 mg, inj. ranitidine 50 mg and inj. hydrocortisone 100 mg were administered. Monitoring included oxygen saturation (SpO 2 ), ECG, non invasive blood pressure (NIBP) and end tidal carbon dioxide (EtCO 2), core temperature from the tympanic membrane. OT temperature was maintained at 22° C. Induction was done with 2.5 mg/kg of propofol and 1.5 μg/kg of fentanyl following preoxygenation and intubated with 7.5 cuffed endotracheal tube using 20 mg of atracurium and neuromuscular monitoring (NM) with Train-of-Four (TOF) ratio. He was maintained on N 2 O in O 2 (66:33), 0.6-0.8% halothane with controlled ventilation and incremental fentanyl 20 μg along with atracurium top-ups of 10 mg using N-M monitoring. I.V. Ringer lactate about 1200 ml was infused. At the conclusion of surgery neuromuscular block was reversed with neostigmine 0.05 mg/kg and glycopyrrolate 0.4 mg satisfactorily. I.V. inj. ondancetron 4 mg was administered.
Post-operatively SpO 2 , NIBP, ECG and temperature monitoring along with O 2 supplementation by ventimask was done in the recovery room. I.V. Tramadol 2 mg/kg, six hourly was used for post-operative analgesia. There was a rise of temperature 1°C, eight hours postoperatively which was treated with I.V. Paracetamol, 10 mg/kg, and cold sponging promptly. Also there was respiratory distress after twelve hours which subsided after increasing O 2 concentration to 60%. He was discharged after 10 days. There was no neurological exacerbation of the disease.
| Discussion | |
MS occurs in genetically susceptible individuals following an environmental, viral exposure that produces activated autoreactive T cells and cytokines, disrupting the blood-brain barrier. [3],[4] The inflammatory process produces demyelination and glial scarring (sclerosis) in scattered areas of brain and spinal cord that leads to conduction blockade along the neural pathways wherein Na + channels are affected by endogenous oligopeptides resembling blockade by local anaesthetics LA. [4] This results in multiple sensory deficits, cranial nerve palsies, limb weakness, paraesthesias, cardiac dysrhythmias, autonomic dysfunction, ventilatory disturbances leading to hypoxaemia and respiratory failure.[1],[2],[3]
Clinically, there are three main type:
- Relapsing-remitting: episodic symptoms with remissions
- Primary progressive: progressive neurologic deterioration without remissions.
- Secondary progressive: chronically progressive with remissions
All the types can eventually develop into a severe progressive course, ultimately leading to fixed neurologic deficits and disability. Pregnancy is associated with improvement in symptoms and relapse can occur in early post-partum months.[2],[3]
Treatment consists of [2],[3]
- During acute attacks, mainly with corticosteroids
- Immunosuppressants/Immunomodulators to prevent progression. Glatiramer acetate mimics structure of myelin, serves decoy for antibodies. Interferon-β leads to immunomodulation.
- Symptomatic:
Paroxysmal pain with carbamezepine,phenytoin,gabapentin.
Spasticity with baclofen, diazepam, dantrolene.
Depression with antidepressants.
Bladder and bowel disturbance with anticho-linergics.
Currently Schwann cell transplantation is under investigation. [2]
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Table 1: Anaesthetic implications of multiple sclerosis | ||||||||||||||||||||||||
| Literature regarding anaesthetic management contains use of general anaesthesia (GA), spinal and epidural techniques. GA and epidural with low concentrations of LA are considered safe. [2],[3],[4] Spinal anaesthesia has been implicated in postoperative exacerbation, [5],[6] so also epidurals with higher concentrations and longer duration. [2],[3] The demyelinated neurons appear susceptible to the neurotoxicity of LA and aggravate the conduction blockade. [4],[5],[6] As regards conduct of G.A no particular agent among induction agents/inhalation agents is preferred. [2],[3] Succinylcholine is best avoided as it can produce hyperkalemia due to denervation sensitivity by upregulation of acetylcholine receptors. sup>[2],[3] The latter can also cause resistance to non-depolarizing blocking agents (NDBA). [7] Sensitivity to NDBAs can also be present due to muscle wasting and use of medications such as baclofen, dantrolene [3],[8] [Table 1]. N-M monitoring is recommended with titration of the NDBA as required for the surgery. [2],[3] Even a 0.5°C rise of temperature can slow the conduction along the demyelinated segment [2],[3],[4] resulting in relapse, hence maintenance of O.T temperature and temperature monitoring is essential. In spite of prolonged periods of immobility, MS patients surprisingly showed the absence of thrombophlebitis and pulmonary embolism (PE) in contrast to other immobile patients suffering from stroke, quadriplegia and flaccid paraplegia.[9] The presence of lower extremity spastic disease in MS patients appears to protect them from thrombophlebitis and PE, as the occurrence of muscle spasms could prevent venous stasis. [9] Cerebral venous thrombosis (CVT) has been reported in MS exacerbation patients who underwent lumbar puncture (L.P) and were receiving I.V. methylprednisolone. [10] Following L.P, high dose corticosteroids are considered as risk factors for CVT and prophylactic anticoagulant treatment may be warranted when other risk factors of CVT also exist. sup>[10] As MRI scan of our patient showed involvement of cervical and upper thoracic segments, to detect autonomic dysfunction preoperatively we tested heart rate response to deep breathing. Pulmonary function tests and blood-gases are recommended in the case of significant respiratory embarrassment. [3] As diminution of respiratory muscle strength cannot be ruled out even without symptoms vigilance during postoperative period is essential. [3],[5] Perioperative steroid supplementation to avoid adrenal suppression has been advocated in patients with recent steroid usage [3] and we used I.V. hydrocortisone 100 mg just before induction as our patient had received steroids recently. Our patient requested for G.A and induction with propofol-fentanyl provided smooth intubation in spite of 65-70% TOF ratio by ED90 dose of atracurium indicating resistance. Intraoperatively TOF ratio-guided top-ups of atracurium provided adequate NM block required for the orthopaedic procedure. Maintenance of O.T temperature to 22°C helped in maintaining normal core temperature. Postoperatively we treated rise of 1°C of body temperature promptly and no relapses occurred in our patient. The postoperative respiratory distress was successfully treated with oxygen therapy by ventimask. The perioperative period was thus uneventful. To summarize, the optimal anaesthetic management of MS requires careful preoperative assessment, awareness towards perioperative care and postoperative exacerbations of MS. The latter invites special attention and recovery room care with appropriate monitors, oxygen therapy/mechanical ventilation is necessary.
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