METHOD: The Cochrane Central Register of Controlled Trials (1996 to Feb 2019) and MEDLINE (1966 to Feb 2019) were searched, including the related randomised control trials and reviewed articles to find unpublished trials or trials not obtained via electronic searches. Inclusion criteria for the studies included comparing recovery time, recording clinician satisfaction, and assessing the adverse effects of ketofol.
RESULTS: Eleven trials consisting of a total of 1274 patients met our criteria and were included in this meta-analysis. Five trials compared ketofol with a single agent, while six trials compared ketofol with combined agents. While comparing between ketofol and a single agent (either ketamine or propofol), ketofol showed significant effect on recovery time (MD: -9.88, 95% CI: - 14.30 to - 5.46; P = 0.0003; I2 = 92%). However, no significant difference was observed while comparing ketofol with combined agents (RR: 0.75, 95% CI: - 6.24 to 7.74; P < 0.001; I2 = 98%). During single-agent comparison, ketofol showed no significant differences in terms of clinician satisfaction (RR: 2.86, 95% CI: 0.64 to 12.69; P = 0.001; I2 = 90%), airway obstruction (RR: 0.72, 95% CI: 0.35 to 11.48; P = 0.81; I2 = 0%), apnoea (RR: 0.9, 95% CI: 0.33 to 2.44; P = 0.88; I2 = 0%), desaturation (RR: 1.11, 95% CI: 0.64 to 1.94; P = 0.28; I2 = 21%), nausea (RR: 0.52, 95% CI: 0.91 to 1.41; P = 0.2; I2 = 38%), and vomiting (RR: 0.63, 95% CI: 0.25 to 1.61; P = 0.18; I2 = 42%). During comparison with combined agents, ketofol was more effective in reducing hypotension (RR: 4.2, 95% CI: 0.2 to 0.85; P = 0.76; I2 = 0%), but no differences were observed in terms of bradycardia (RR: 0.70, 95% CI: 0.14 to 03.63; P = 0.09; I2 = 53%), desaturation (RR: 1.9, 95% CI: 0.15 to 23.6; P = 0.11; I2 = 61%), and respiratory depression (RR: 1.98, 95% CI: 0.18 to 21.94; P = 0.12; I2 = 59%).
CONCLUSION: There is low certainty of evidence that ketofol improves recovery time and moderate certainty of evidence that it reduces the frequency of hypotension. There was no significant difference in terms of other adverse effects when compared to other either single or combined agents.
TRIAL REGISTRATION: PROSPERO CRD42019127278 .
METHODS: We searched the Cochrane Central Register of Controlled Trials and Epistemonikos, as well as MEDLINE from 1966 till August 2019. Screening of full texts, evaluation for eligibility, and data extraction were done by four independent reviewers. We estimated risk ratios (RR) and mean differences (MD) using a random-effects model with 95% confidence intervals (CI). The primary outcomes included the number of participants who achieved the target mean arterial pressure (MAP), time to achieve the target MAP, and number of participants with all-cause 28-day mortality. The secondary outcomes included the length of stay in the intensive care unit, length of hospital stay, incidence of arrhythmia and myocardial infarction, vasopressor-free days, and number of participants with all-cause 90-day mortality.
RESULTS: We identified 11 randomized controlled trials with a total of 4,803 participants. There was no difference in the number of participants who achieved the target MAP between those patients receiving norepinephrine and other vasopressors (RR 1.44; 95% CI, 0.32 to 6.54; P = 0.640; I2 = 94%; two trials, 116 participants). There was no significant difference in time to achieve the target MAP (MD -0.05; 95%, CI, -0.32 to 0.21; P = 0.690; I2 = 26%; two trials, 1763 participants) and all-cause 28-day mortality (RR 0.95; 95% CI, 0.89 to 1.02; P = 0.160; I2 = 0%; seven trials, 4,139 participants). Regarding the secondary outcome, norepinephrine may significantly reduce the incidence of arrhythmia as compared to other vasopressors (RR 0.64; 95% CI, 0.42 to 0.97; P = 0.030; I2 = 64%; six trials, 3974 participants). There was no difference in the incidence of myocardial infarction (RR 1.28; 95% CI, 0.79 to 2.09), vasopressor-free day (RR 0.46; 95% CI, -1.82 to 2.74) and all-cause 90-day mortality (RR 1.08; 95% CI, 0.96 to 1.21) between norepinephrine and vasopressors.
CONCLUSION: In minimizing the occurrence of an arrhythmia, norepinephrine is superior to other vasopressors, making it safe to be used in septic shock. However, there was insufficient evidence concerning mortality and achievement of the target MAP outcomes.
METHODS: We searched databases Cochrane Central Register of Controlled Trials (CENTRAL), Medline and Google Scholar up to January 2021 and identified randomised controlled trials comparing ketorolac to any other medications in treating patients presenting with migraine headache.
RESULTS: Thirteen trials were included in our review, comprising of 944 participants. We derived seven comparisons; ketorolac versus phenothiazines, metoclopramide, sumatriptan, dexamethasone, sodium valproate, caffeine, and diclofenac. There were no significant differences in the reduction of pain intensity at 1-hour under the comparisons between ketorolac and phenothiazines (standard mean difference (SMD) 0.09, P 0.74), or metoclopramide (SMD 0.02, P 0.95). We also found no difference in the outcome recurrence of headache [ketorolac vs phenothiazines (risk ratio (RR) 0.98, P 0.97)], ability to return to work or usual activity [ketorolac vs metoclopramide (RR 0.64, P 0.13)], need for rescue medication [ketorolac vs phenothiazines (RR 1.72, P 0.27), ketorolac vs metoclopramide (RR 2.20, P 0.18)], and frequency of adverse effects [ketorolac vs metoclopramide (RR 1.07, P 0.82)]. Limited trials suggested that ketorolac offered better pain relief at 1-hour compared to sumatriptan and dexamethasone, had lesser frequency of adverse effects than phenothiazines, and was superior to sodium valproate in terms of reduction of pain intensity at 1-hour, need for rescue medication and sustained headache freedom within 24-hour.
CONCLUSIONS: Ketorolac may have similar efficacy to phenothiazines and metoclopramide in treating acute migraine headache. Ketorolac may also offer better pain control than sumatriptan, dexamethasone and sodium valproate. However, given the lack of evidence due to inadequate number of trials available, future studies are warranted.
Methods: This cross-sectional study involved patients over age 3 years old who presented with URTI to the green zone of the ED of a tertiary hospital on the east coast of Malaysia in 2018-2019. Convenient sampling was done. The patients were categorised into two groups according to their McIsaac scores: positive (≥ 2) or negative (< 2). Antibiotics given to the negative McIsaac group were considered inappropriate.
Results: A total of 261 cases were included - 127 with positive and 134 with negative McIsaac scores. The most common symptoms were fever and cough. About 29% had inappropriate antibiotic prescribing with a high rate for amoxycillin. Duration of symptoms of one day or less (OR 18.5; 95% CI: 1.65, 207.10; P = 0.018), presence of chills (OR 4.36; 95% CI: 1.13, 16.88; P = 0.033) and diagnosis of acute tonsillitis (OR 5.26; 95% CI: 1.76, 15.72; P = 0.003) were significantly associated with inappropriate antibiotic prescription.
Conclusion: Factors influencing inappropriate antibiotic prescribing should be pointed out to emergency doctors to reduce its incidence.