Paroxysmal autonomic instability with dystonia (PAID) appears to be a unique syndrome following brain injury. It can echo many life-threatening conditions, making its early recognition and management a challenge for intensivists. A delay in early recognition and subsequent management may result in increased morbidity, which is preventable in affected patients. Herein, we report the case of a patient who was diagnosed with PAID syndrome following prolonged cardiac arrest, and discuss the pathophysiology, clinical presentation and management of this rare and under-recognised clinical entity.
Adult ; Anxiety ; complications ; Autonomic Nervous System Diseases ; etiology ; Brain Injuries ; etiology ; Critical Care ; Diagnosis, Differential ; Dystonia ; etiology ; Heart Arrest ; complications ; Humans ; Hypoxia ; Male ; Respiration Disorders ; complications ; Syndrome ; Treatment Outcome

Background: No meta-analysis has holistically analysed and summarised the efficacy and safety of gemigliptin in type 2 diabetes. The meta-analysis addresses this knowledge gap. Methods: Electronic databases were searched for randomised controlled trials (RCTs) involving diabetes patients receiving gemigliptin in the intervention arm and placebo/active comparator in the control arm. The primary outcome was change in haemoglobin A1c (HbA1c). The secondary outcomes were alterations in glucose, glycaemic targets, lipids, insulin resistance, and adverse events. Results: Data from 10 RCTs involving 1,792 patients were analysed. Four had an active control group (ACG), with metformin/dapagliflozin/sitagliptin/glimepiride as the active comparator; six had a passive control group (PCG), with placebo/rosuvastatin as controls. HbA1c reduction by gemigliptin at 24 weeks was comparable to ACG (mean difference [MD], 0.09%; 95% confidence interval [CI], –0.06 to 0.23; P=0.24; I2=0%; moderate certainty of evidence [MCE]), but superior to PCG (MD, –0.91%; 95% CI, –1.18 to –0.63); P<0.01; I2=89%; high certainty of evidence [HCE]). Gemigliptin was superior to PCG regarding achieving HbA1c <7% (12 weeks: odds ratio [OR], 5.91; 95% CI, 1.34 to 26.08; P=0.02; I2=74%; 24 weeks: OR, 4.48; 95% CI, 2.09 to 9.60; P<0.01; I2=69%; HCE). Gemigliptin was comparable to ACG regarding achieving HbA1c <7% after 24 weeks (OR, 0.92; 95% CI, 0.52 to 1.63; P=0.77; I2=66%; MCE). Adverse events were similar between the gemigliptin and control groups (risk ratio [RR], 1.06; 95% CI, 0.82 to 1.36; P=0.66; I2=35%; HCE). The gemigliptin group did not have increased hypoglycaemia (RR, 1.19; 95% CI, 0.62 to 2.28; P=0.61; I2=19%; HCE). Conclusion Gemigliptin has good glycaemic efficacy and is well-tolerated over 6 months of use.

Background: No meta-analysis has holistically analysed and summarised the efficacy and safety of gemigliptin in type 2 diabetes. The meta-analysis addresses this knowledge gap. Methods: Electronic databases were searched for randomised controlled trials (RCTs) involving diabetes patients receiving gemigliptin in the intervention arm and placebo/active comparator in the control arm. The primary outcome was change in haemoglobin A1c (HbA1c). The secondary outcomes were alterations in glucose, glycaemic targets, lipids, insulin resistance, and adverse events. Results: Data from 10 RCTs involving 1,792 patients were analysed. Four had an active control group (ACG), with metformin/dapagliflozin/sitagliptin/glimepiride as the active comparator; six had a passive control group (PCG), with placebo/rosuvastatin as controls. HbA1c reduction by gemigliptin at 24 weeks was comparable to ACG (mean difference [MD], 0.09%; 95% confidence interval [CI], –0.06 to 0.23; P=0.24; I2=0%; moderate certainty of evidence [MCE]), but superior to PCG (MD, –0.91%; 95% CI, –1.18 to –0.63); P<0.01; I2=89%; high certainty of evidence [HCE]). Gemigliptin was superior to PCG regarding achieving HbA1c <7% (12 weeks: odds ratio [OR], 5.91; 95% CI, 1.34 to 26.08; P=0.02; I2=74%; 24 weeks: OR, 4.48; 95% CI, 2.09 to 9.60; P<0.01; I2=69%; HCE). Gemigliptin was comparable to ACG regarding achieving HbA1c <7% after 24 weeks (OR, 0.92; 95% CI, 0.52 to 1.63; P=0.77; I2=66%; MCE). Adverse events were similar between the gemigliptin and control groups (risk ratio [RR], 1.06; 95% CI, 0.82 to 1.36; P=0.66; I2=35%; HCE). The gemigliptin group did not have increased hypoglycaemia (RR, 1.19; 95% CI, 0.62 to 2.28; P=0.61; I2=19%; HCE). Conclusion Gemigliptin has good glycaemic efficacy and is well-tolerated over 6 months of use.

Background: Dynamic parameters used for predicting fluid responsiveness require special equipment and are minimally invasive. Therefore, recent interest in the use of carotid artery ultrasound parameters, such as carotid corrected flow time (FTc) and peak velocity variation (ΔVpeak) has grown. Therefore, we performed this systematic review and meta-analysis to assess the ability of carotid FTc and/or ΔVpeak to accurately predict fluid responsiveness. Methods: We searched the PubMed and Embase databases for articles evaluating the diagnostic accuracy of carotid FTc or ΔVpeak for predicting fluid responsiveness. Two independent authors performed the search and selected studies published until May 2022. The studies were assessed for the inclusion and exclusion criteria using Rayyan (Rayyan Systems Inc., 2022). Results: Ten studies (n=438) that fulfilled the inclusion criteria were selected. Studies were divided into those assessing carotid FTc and those assessing carotid ΔVpeak. Five studies (six datasets) assessed FTc. The pooled sensitivity and specificity of carotid FTc were 0.76 and 0.88, respectively. The summary receiver operating characteristic (SROC) curve for carotid FTc had an area under the curve (AUC) of 0.9092, with a Q value of 0.8412. Seven studies calculated carotid ΔVpeak. The pooled sensitivity and specificity for ΔVpeak were 0.83 and 0.81, respectively. The SROC curve had an AUC of 0.8941 and a Q value of 0.8250. Conclusions Our meta-analysis showed that both carotid FTc and ΔVpeak are useful for predicting fluid responsiveness in anesthesia and critical care settings with good specificity and sensitivity.

Pediatric glioblastoma (pGBM) is a rare entity accounting for only approximately 3% of all childhood brain tumors. Treatment guidelines for pGBM have been extrapolated from those in adult glioblastoma. Rarity of pGBM and underrepresentation of pediatric population in major studies precludes from defining the ideal treatment protocol for these patients. Maximum safe resection is performed in most of the cases followed by postoperative radiotherapy in children over 3 years of age. Benefit of temozolomide is unclear in these patients. Here, we present the clinicopathological details and outcome of six pGBM patients treated at our institute in 2018–2019.

Pediatric glioblastoma (pGBM) is a rare entity accounting for only approximately 3% of all childhood brain tumors. Treatment guidelines for pGBM have been extrapolated from those in adult glioblastoma. Rarity of pGBM and underrepresentation of pediatric population in major studies precludes from defining the ideal treatment protocol for these patients. Maximum safe resection is performed in most of the cases followed by postoperative radiotherapy in children over 3 years of age. Benefit of temozolomide is unclear in these patients. Here, we present the clinicopathological details and outcome of six pGBM patients treated at our institute in 2018–2019.