Association between intraoperative hyperglycemia and postoperative end-organ dysfunctions after cardiac surgery: a retrospective observational study.

PURPOSE: Hyperglycemia has been associated with postoperative morbidity in patients who undergo cardiac surgery. However, it remains unclear whether the duration of hyperglycemia is as important as its magnitude in the development of postoperative end-organ dysfunction (PEOD). This retrospective study investigated the hypothesis that the intraoperative blood glucose (BG) exposure index (GE index), calculated by the product of the magnitude and duration of BG concentration ≥ 180 mg/dL, which is an integration of the severity and duration of hyperglycemia, is associated with the incidence of PEOD in patients undergoing cardiac surgery with cardiopulmonary bypass. METHODS: The primary outcome in this study was PEOD within 72 h of surgery, which was defined as a composite of postoperative acute kidney injury, delirium, myocardial injury, and prolonged mechanical ventilation. The GE index (the magnitude of BG concentration deviation ≥ 180 mg/dL [Formula: see text] duration of BG concentration ≥ 180 mg/dL) of each patient was calculated based on the intraoperative BG concentration. The relationship between the GE index and the primary outcome was examined via logistic regression model with adjustment for potential confounders. RESULTS: Within 72 h of surgery, 301 patients (54.5%) developed PEOD. PEOD was more common in patients with greater GE index quartiles (first versus third quartile; adjusted odds ratio, 5.65, 95% confidence interval (95% CI), 2.94-10.90; P < 0.001; first versus forth quartile, adjusted odds ratio, 20.80; 95% CI, 8.01-54.00; P < 0.001). CONCLUSION: In patients undergoing cardiac surgery with cardiopulmonary bypass, the GE index was an independent predictor of PEOD.

Factors for Acute Kidney Injury Following Total Arch Replacement and Association with Temperature Management During Cardiopulmonary Bypass: A Single-center Retrospective Observational Study.

Many patients develop acute kidney injury (AKI) after vascular surgery. In this retrospective observational study, we investigated the risk factors for AKI defined using the Kidney Disease Improving Global Outcomes criteria after total arch replacement (TAR). Additionally, we investigated the influence of temperature manage-ment during cardiopulmonary bypass (CPB) on postoperative renal function by propensity score-matched anal-ysis. We retrospectively analyzed 161 consecutive patients who underwent TAR between 2016 and 2019. Postoperative AKI occurred in 48.7% of the patients. In the multivariate analysis, male sex (odds ratio [OR] 3.95, 95% confidence interval [95%CI] 1.56-8.27, p = 0.002), ACE inhibitors/ARB medication (OR 3.19, 95%CI 1.49-6.82, p = 0.003), preoperative chronic kidney disease (OR 2.47, 95%CI 1.17-5.23, p = 0.02), pro-longed CPB time (OR 2.36, 95%CI 1.05-5.34, p = 0.04), and lower body ischemic time during CPB (OR 2.20, 95%CI 1.05-4.46, p = 0.04) were identified as independent risk factors for AKI. Propensity score-matched anal-ysis showed no significant difference in the risk of AKI following TAR between mild hypothermia or normo-thermia and moderate hypothermia (37.2% vs. 41.9%, p = 0.83). In conclusion, modifiable risk factors for AKI included prolonged CPB time and lower body ischemic time. Temperature management during CPB had no clear effect on outcomes.

Management of an 11-year-old patient who presented with acute aortic dissection.

An 11-year-old boy with no medical or family history was diagnosed with Stanford type B acute aortic dissection. Although a conservative treatment approach was adopted, deep sedation was required to keep him still during computed tomography. It revealed enlargement of the false lumen of the descending aorta, bilateral pleural effusion, and atelectasis. Thus, he underwent descending aortic replacement. After amelioration of perioperative rhabdomyolysis, he was discharged post-recovery. Since there have been no clinical guidelines for management of pediatric aortic dissection, it was difficult to decide between surgical and conservative approaches. Considering difficulty of mild sedation in children, if conservative approaches seem to be problematic, an early surgical approach with aortic replacement is sometimes necessary. .

Quercetin Attenuates Neuropathic Pain in Rats with Spared Nerve Injury.

Quercetin is a flavonoid widely found in plants and marketed to the public as a supplement. Several studies have reported its effect on glial cells. This study aimed to examine the effect of quercetin on the development of neuropathic pain and the underlying mechanism in a spared nerve injury (SNI) rat model. Male Sprague-Dawley rats randomly assigned to the control or the quercetin group were subjected to SNI of the sciatic nerve. We measured pain behaviors on the hind paw and glial fibrillary acidic protein (GFAP) in the dorsal root ganglion (DRG) and spinal cord. Oral administration of 1% quercetin, begun before surgery, attenuated mechanical allodynia compared to the control group at days 7 and 10 after SNI. On the other hand, established pain was not attenuated in a post-dose group in which quercetin was begun 7 days after SNI. Quercetin inhibited GFAP in the satellite glial cells of the ipsilateral L5 DRG on day 7 compared to the control group. Quercetin suppressed the development of neuropathic pain through a mechanism partly involving the inhibition of satellite glial cells. As its safety is well established, quercetin has great potential for clinical use in pain treatment.

Erratum to: Preoperative brain magnetic resonance imaging and postoperative delirium after off-pump coronary artery bypass grafting: a prospective cohort study.

Erratum to: Can J Anesth/J Can Anesth DOI 10.1007/s12630-015-0327-x. In the published version, the first name of the third author is incorrect and should read Naoaki Yamada as given in this erratum. The publisher apologizes most sincerely for this error.

Preoperative brain magnetic resonance imaging and postoperative delirium after off-pump coronary artery bypass grafting: a prospective cohort study.

BACKGROUND: Delirium after cardiac surgery is a serious complication, increasing morbidity and mortality. Despite its high expectations, off-pump coronary artery bypass grafting (OPCAB) has largely failed to reduce the incidence of postoperative neurological complications. To further investigate the reasons for this failure, we used perioperative brain magnetic resonance imaging (MRI) to determine the relation between MRI findings and postoperative delirium. METHODS: Altogether, 98 patients undergoing elective OPCAB were enrolled in this prospective observational study. Patients underwent brain MRI and magnetic resonance angiography (MRA) before and after surgery to identify cerebral infarction, white matter lesions, and intracranial artery stenosis. Postoperative delirium in the intensive care unit was measured using the delirium rating scale. The relation between postoperative delirium and MRI findings was examined using logistic regression. RESULTS: Magnetic resonance imaging and MRA was completed in 88 (90%) of the patients. New ischemic lesions were present in seven (7.9%) patients. Delirium rating scale scores of 0, 1-7, and ≥ 8 were found in 25 (31%), 48 (60%), and seven (9%) patients, respectively. Multivariate logistic regression analysis revealed that new ischemic lesions (odds ratio [OR] 11.07, 95% confidence interval [CI]: 1.53 to 80.03; P = 0.017), carotid artery stenosis (OR 7.06, 95% CI: 1.59 to 31.13; P = 0.010), history of myocardial infarction (OR 3.78, 95% CI: 1.05 to 13.65; P = 0.043), and deep subcortical white matter hyperintensity (OR 3.04, 95% CI: 1.14 to 8.12; P = 0.027) were significantly associated with postoperative delirium. CONCLUSIONS: Magnetic resonance imaging findings of new cerebral ischemic lesions, carotid stenosis, and deep subcortical white matter hyperintensity correlated significantly with postoperative delirium in patients who had undergone OPCAB surgery.

Up-regulation of brain-derived neurotrophic factor in the dorsal root ganglion of the rat bone cancer pain model.

Metastatic bone cancer causes severe pain, but current treatments often provide insufficient pain relief. One of the reasons is that mechanisms underlying bone cancer pain are not solved completely. Our previous studies have shown that brain-derived neurotrophic factor (BDNF), known as a member of the neurotrophic family, is an important molecule in the pathological pain state in some pain models. We hypothesized that expression changes of BDNF may be one of the factors related to bone cancer pain; in this study, we investigated changes of BDNF expression in dorsal root ganglia in a rat bone cancer pain model. As we expected, BDNF mRNA (messenger ribonucleic acid) and protein were significantly increased in L3 dorsal root ganglia after intra-tibial inoculation of MRMT-1 rat breast cancer cells. Among the eleven splice-variants of BDNF mRNA, exon 1-9 variant increased predominantly. Interestingly, the up-regulation of BDNF is localized in small neurons (mostly nociceptive neurons) but not in medium or large neurons (non-nociceptive neurons). Further, expression of nerve growth factor (NGF), which is known as a specific promoter of BDNF exon 1-9 variant, was significantly increased in tibial bone marrow. Our findings suggest that BDNF is a key molecule in bone cancer pain, and NGF-BDNF cascade possibly develops bone cancer pain.

Spinal nerve injury causes upregulation of ErbB2 and ErbB3 receptors in rat dorsal root ganglia.

It is generally known that peripheral nerve injury causes changes in expression of some growth factors in the dorsal root ganglion. Altered expression of ErbB receptors, a well-known growth factor in somatic cells, reportedly follows peripheral nerve injury in the spinal dorsal horn; however, it remains unknown whether the expression of these receptors is altered in the dorsal root ganglion after nerve injury. Therefore, this study examined the gene expression profiles of ErbB receptors in bilateral lumbar (L)4/L5 dorsal root ganglia, using L5-selective spinal nerve ligation in model rats as a peripheral nerve injury model. The expression of ErbB2 and ErbB3 was observed in the dorsal root ganglia of the mature rat, despite ErbB1 and ErbB4 showing only subtle expression. We also demonstrated that peripheral nerve injury induced significant increases in ErbB2 and ErbB3 in the ipsilateral dorsal root ganglion as compared with uninjured nerve. Expression changes in ErbB receptors appear to play important roles in nerve injury and subsequent nerve regeneration.