Background and Aims:Use of various adjuvants to spinal anaesthesia is a well-known modality to provide intra- and post-operative analgesia. This study was designed to evaluate and compare the analgesic efficacy of clonidine and magnesium when used as an additive to intrathecal 0.5% hyperbaric bupivacaine.Methods:Ninety patients of the American Society of Anesthesiologists’ physical status grade I or II, scheduled for lower abdominal surgery under spinal anaesthesia, were randomly allocated into three groups. Group B received 3 mL of 0.5% hyperbaric bupivacaine with 1 mL of normal saline, Group C received 3 mL of 0.5% hyperbaric bupivacaine with 1 mL (30 μg) of clonidine and Group M received 3 mL of 0.5% hyperbaric bupivacaine with 1 mL (50 mg) magnesium sulphate. The primary outcome variable was duration of analgesia and secondary outcome variables included onset and duration of sensory and motor block, sedation level and adverse effects. Data were analysed with ANOVA, Kruskal–Wallis and Chi-square tests.Results:The time to first rescue analgesia was significantly (P < 0.01) longer in the Group C (330.7 ± 47.7 min) than both Groups. Group M (246.3 ± 55.9 min) showed significantly prolonged analgesia than Group B (134.4 ± 17.9 min). Group C and Group M showed significantly prolonged duration of both sensory and motor block compared to Group B.Conclusion:Intrathecal clonidine added to bupivacaine prolongs the duration of post-operative analgesia, and hastens the onset and prolongs the duration of sensory and motor block compared to magnesium or controls.

Introduction: The COVID-19 pandemic is a global crisis, the number of cases and deaths are on a steep incline. This article reviews the possible immunological mechanisms which underlie the disease pathogenesis by looking at the behaviour of previous coronaviruses not only in humans but also other mammals which possibly act as reservoir hosts. Observations: A key aspect of this coronavirus as well as the previous SARS CoV seems to be the importance of host immune response in the pathology and clinical severity of illness caused by them. A hyperactive innate immune state in combination with an exhausted adaptive immune response are possible determinants of severe illness. Conclusion: There is a possibility that the current SARS CoV 2 has immune evasive tactics similar to SARS CoV in its repertoire, since they share a 76% homology. These might have been learnt behaviour from long periods of persistence in their reservoir hosts and they may be the reason behind the dysregulated immune response evoked in humans. That in turn is highly likely to be one of the factors which govern disease severity. With this in mind we want to bring the medical community&rsquo;s attention to a &lsquo;hit early, hit hard&rsquo; intervention as a possible strategy to modify the course of the disease and bring down the numbers of severe sufferers.

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