MATERIALS AND METHODS: Eighty patients for laparoscopic surgery with at least one of the determined risks (nonsmoker, female, previous PONV/motion sickness, or postoperative opioid use) were randomized into either an active or sham group. At the end of surgery, Reletex electrical acustimulation was placed at the P6 acupoint. The active group had grade 3 strength and the sham group had inactivated electrodes covered by silicone. It was worn for 24 h following surgery. PONV scores were recorded.
RESULTS: The active group had significantly shorter durations of surgery and lower PONV incidence over 24 h (35.1% versus 64.9%, P = 0.024) and this was attributed to the lower incidence of nausea (31.4% versus 68.6%, P = 0.006). The overall incidence of vomiting was not significantly different between the groups, but it was higher in the sham group of patients with PONV risk score 3 (23.9%, P = 0.049).
CONCLUSION: In patients at high risk for PONV, P6 acupoint electrical stimulation lowers the PONV incidence by reducing the nausea component. However, this reduction in nausea is not related to increasing PONV risk scores.
METHODS: In three double-blind phase 3 studies, patients receiving HEC or MEC were randomized 1:1 to receive oral rolapitant 180 mg or placebo prior to chemotherapy plus 5-hydroxytryptamine type 3 receptor antagonist and dexamethasone therapy. Patients completed the FLIE questionnaire on day 6 of cycle 1. Endpoints included FLIE total score, nausea and vomiting domain scores, and the proportion of patients with no impact on daily life (total score >108 [range 18-126]). We performed a prespecified analysis of the MEC/anthracycline-cyclophosphamide (AC) study and a post hoc analysis of two pooled cisplatin-based HEC studies.
RESULTS: In the pooled HEC studies, rolapitant significantly improved the FLIE total score (114.5 vs 109.3, p nausea score (55.3 vs 53.5, p nausea score (54.1 vs 52.3, p
STUDY DESIGN: Randomised controlled trial.
SETTING: Tertiary level hospital in Malaysia.
PATIENTS: 77 patients undergoing elective Caesarean delivery.
INTERVENTION: Differing speeds of spinal injection.
MEASUREMENTS: Systolic blood pressure was assessed every minute for the first 10min and incidence of hypotension (reduction in blood pressure of >30% of baseline) was recorded. The use of vasopressor and occurrence of nausea/vomiting were also recorded.
MAIN RESULTS: 36 patients in SLOW group and 41 patients in FAST group were recruited into the study. There was no significant difference in blood pressure drop of >30% (p=0.497) between the two groups. There was no difference in the amount of vasopressor used and incidence of nausea/vomiting in both groups.
CONCLUSION: In our study population, there was no difference in incidence of hypotension and nausea/vomiting when spinal injection time is prolonged beyond 15s to 60s.
TRIAL REGISTRATION: ClinicalTrials.govNCT02275897. Registered on 15 October 2014.
METHODS: Sixty patients were randomised to receive IV dexmedetomidine 0.5 μg.kg-1 (Group DEX, n = 30) or IV saline (Group P, n = 30). General anaesthesia was maintained with Sevoflurane: oxygen: air, titrated to BIS 40-60. Pain intensity, sedation, rescue analgesics, nausea/vomiting and resumption of daily activities were recorded at 1 h, and postoperative day (POD) 1-5.
RESULTS: Group DEX patients had significant reduction in sevoflurane minimum alveolar concentration (MAC), mean (SD) DEX vs. Placebo 0.6 (0.2) vs. 0.9 (0.1), p = 0.037; reduced postoperative resting pain at 1 h (VAS 0-10) (mean (SD) 1.00 (1.84) vs. 2.63 (2.78), p = 0.004), POD 1 (mean (SD) 1.50 (1.48) vs. 2.87 (2.72), p = 0.002), POD 2 (0.53 (0.97) vs. 1.73 (1.96), p = 0.001) and POD 3 (0.30 (0.75) vs. 0.89 (1.49), p = 0.001). DEX patients also had less pain on movement POD 1 (3.00 (2.12) vs. 4.30 (3.10), p = 0.043) and POD 2 (2.10 (1.98) vs. 3.10 (2.46), p = 0.040), with higher resumption of daily activities by 48 h compared to placebo, 87% vs. 63%, p = 0.04.
CONCLUSIONS: We conclude that a single dose of dexmedetomidine was a useful adjuvant in reducing MAC and postoperative pain (at 1 h and POD 1-3), facilitating faster return to daily activities by 48 h.
TRIAL REGISTRATION: The Australian New Zealand Clinical Trials Registry (ANZCTR), ACTRN12617001120369 , 31st July 2017, retrospectively registered.
Methods: A single-centre, retrospective study evaluating posaconazole Cmin in LTx recipients receiving posaconazole suspension or MR tablets between January 2014 and December 2016.
Results: Forty-seven LTx patients received posaconazole suspension, and 78 received the MR tablet formulation; a total of 421 and 617 Cmin measurements were made, respectively. Posaconazole was concurrently administered with proton pump inhibitor in ≥ 90% of patients. The median (IQR) of initial posaconazole Cmin following 300 mg daily of posaconazole tablet was significantly higher than that of 800 mg daily of posaconazole suspension [1.65 (0.97-2.13) mg/L versus 0.81 (0.48-1.15) mg/L, P nausea/vomiting and weight loss) were reported in 3/78 (4%) patients receiving posaconazole MR tablets. Posaconazole Cmin in these three patients was determined to be 9.6, 6.2 and 2.3 mg/L.
Conclusions: The current study has provided clinically important insights into the TDM of posaconazole in LTx recipients. Routine TDM should be undertaken in LTx recipients receiving posaconazole suspension and/or MR tablets.
PATIENT CONCERNS: A 61-year-old Asian female with underlying type 2 DM presented to our ED with body weakness, dyspnea, nausea, vomiting, and mild abdominal pain for the past 2 days. These symptoms were preceded by poor oral intake for 1 week due to severe toothache. Dapagliflozin was recently added to her antidiabetic drug regimen of metformin and glibenclamide 2 weeks ago.
DIAGNOSES: Arterial blood gases showed a picture of severe metabolic acidosis with an elevated anion gap, while ketones were elevated in blood and positive in urine. Blood glucose was mildly elevated at 180 mg/dL. Serum lactate levels were normal. Our patient was thus diagnosed with eDKA.
INTERVENTION: Our patient was promptly admitted to the intensive care unit and treated for eDKA through intravenous rehydration therapy with insulin infusion.
OUTCOMES: Serial blood gas analyses showed gradual resolution of the patient's ketoacidosis with normalized anion gap and clearance of serum ketones. She was discharged uneventfully on day 4, with permanent cessation of dapagliflozin administration.
LESSONS: Life-threatening eDKA as a complication of dapagliflozin is a challenging and easilymissed diagnosis in the ED. Such an ED presentation is very rare, nevertheless emergency physicians are reminded to consider the diagnosis of eDKA in a patient whose drug regimen includes any SGLT2 inhibitor, especially if the patient presents with nausea, vomiting, abdominal pain, dyspnea, lethargy, and is clinically dehydrated. These patients should then be investigated with ketone studies and blood gas analyses regardless of blood glucose levels for prompt diagnosis and treatment.
DESIGN: 1805 consecutive unselected patients with FGID who presented for primary or secondary care to 11 centres across Asia completed a cultural and linguistic adaptation of the Rome III Diagnostic Questionnaire that was translated to the local languages. Principal components factor analysis with varimax rotation was used to identify symptom clusters.
RESULTS: Nine symptom clusters were identified, consisting of two oesophageal factors (F6: globus, odynophagia and dysphagia; F9: chest pain and heartburn), two gastroduodenal factors (F5: bloating, fullness, belching and flatulence; F8 regurgitation, nausea and vomiting), three bowel factors (F2: abdominal pain and diarrhoea; F3: meal-related bowel symptoms; F7: upper abdominal pain and constipation) and two anorectal factors (F1: anorectal pain and constipation; F4: diarrhoea, urgency and incontinence).
CONCLUSION: We found that the broad categorisation used both in clinical practice and in the Rome system, that is, broad anatomical divisions, and certain diagnoses with long historical records, that is, IBS with diarrhoea, and chronic constipation, are still valid in our Asian societies. In addition, we found a bowel symptom cluster with meal trigger and a gas cluster that suggests a different emphasis in our populations. Future studies to compare a non-Asian cohort and to match to putative pathophysiology will help to verify our findings.
A 53-year-old woman presented with left-sided abdominal pain, nausea and vomiting for the past 3 months with associated loss of appetite and weight. On physical examination, there was a large, ill-defined, firm mass at the epigastrium. Ultrasonography showed heterogeneously hypoechoic filling defect within the dilated main portal vein. The filling defect showed florid signals on Doppler mode and it appeared to be an extension of a larger periportal mass. Contrast enhanced abdominal computed tomography confirmed a large distal gastric mass infiltrating into the periportal structures, including the main portal vein and the splenic vein. Esophagogastroduodenoscopy performed 2 days later showed an irregular, exophytic mass extending from the antrum into the first part of duodenum. The mass was deemed inoperable. Histopathological examination showed gastric adenocarcinoma. She was started on anticoagulant, chemotherapy and pain management. Follow-up computed tomography 4 months later showed liver metastases and formation of collateral blood vessels.
METHODS: Using a decision tree model, clinical and economic outcomes associated with olanzapine-containing regimen and standard antiemetic regimen (doublet antiemetic regimen: dexamethasone+first generation 5HT3RA) in most SEA countries except in Singapore (triplet antiemetic regimen: dexamethasone+first generation 5HT3RA + aprepitant) for CINV prevention following HEC were evaluated. This analysis was performed in Thailand, Malaysia, Indonesia, and Singapore, using societal perspective method with 5-day time horizon. Input parameters were derived from literature, network meta-analysis, government documents, and hospital databases. Outcomes were incremental cost-effectiveness ratio (ICER) in USD/quality-adjusted life year (QALY) gained. A series of sensitivity analyses including probabilistic sensitivity analysis were also performed.
RESULTS: Compared to doublet antiemetic regimen, addition of olanzapine resulted in incremental QALY of 0.0022-0.0026 with cost saving of USD 2.98, USD 27.71, and USD 52.20 in Thailand, Malaysia, and Indonesia, respectively. Compared to triplet antiemetic regimen, switching aprepitant to olanzapine yields additional 0.0005 QALY with cost saving of USD 60.91 in Singapore. The probability of being cost-effective at a cost-effectiveness threshold of 1 GDP/capita varies from 14.7 to 85.2% across countries.
CONCLUSION: The use of olanzapine as part of standard antiemetic regimen is cost-effective for the prevention of CINV in patients receiving HEC in multiple SEA countries.