Haeng Seon Shim

Potentially modifiable risk factors for acute kidney injury after surgery on the thoracic aorta: a propensity score matched case-control study.

Abstract Perioperative risk factors were identified for acute kidney injury (AKI) defined by the RIFLE criteria (RIFLE = risk, injury, failure, loss, end stage) after surgery on the thoracic aorta with cardiopulmonary bypass (CPB) in this case-control study. A retrospective review was completed for 702 patients who underwent surgery on the thoracic aorta with CPB. A total of 183 patients with AKI were matched 1:1 with patients without AKI by a propensity score. Matched variables included age, gender, body-mass index, preoperative creatinine levels, estimated glomerular filtration rate, a history of hypertension, diabetes mellitus, cerebrovascular accident, smoking history, or chronic obstructive pulmonary disease to exclude the influence of patient demographics, preoperative medical status, and baseline renal function. Multivariate logistic regression analysis was used to evaluate for independent risk factors in the matched sample of 366 patients. The incidence of AKI was 28.6% and 5.9% of patients from the entire sample required renal replacement therapy. AKI was associated with a prolonged postoperative hospital stay and a higher one-month and one-year mortality both in the entire and matched sample set. Independent risk factors for AKI were a left ventricular ejection fraction <55%, preoperative hemoglobin level <10 g/dL, albumin <4.0 g/dL, diagnosis of dissection, operation time >7 hours, deep hypothermic circulatory arrest (DHCA) time >30 min, pRBC transfusion >1000 mL, and FFP transfusion >500 mL. Although the incidence of poor glucose control (blood glucose >180 mg/dL) was higher in patients with AKI in matched sample, it was not an independent risk factor. AKI was still associated with a poor clinical outcome in the matched sample. Potentially modifiable risk factors included preoperative anemia and hypoalbuminemia. Efforts to minimize operation time and DHCA time along with transfusion amount may protect patients undergoing aortic surgery against AKI.

Clinical Risk Scoring Models for Prediction of Acute Kidney Injury after Living Donor Liver Transplantation: A Retrospective Observational Study.

Acute kidney injury (AKI) is a frequent complication of liver transplantation and is associated with increased mortality. We identified the incidence and modifiable risk factors for AKI after living-donor liver transplantation (LDLT) and constructed risk scoring models for AKI prediction. We retrospectively reviewed 538 cases of LDLT. Multivariate logistic regression analysis was used to evaluate risk factors for the prediction of AKI as defined by the RIFLE criteria (RIFLE = risk, injury, failure, loss, end stage). Three risk scoring models were developed in the retrospective cohort by including all variables that were significant in univariate analysis, or variables that were significant in multivariate analysis by backward or forward stepwise variable selection. The risk models were validated by way of cross-validation. The incidence of AKI was 27.3% (147/538) and 6.3% (34/538) required postoperative renal replacement therapy. Independent risk factors for AKI by multivariate analysis of forward stepwise variable selection included: body-mass index >27.5 kg/m2 [odds ratio (OR) 2.46, 95% confidence interval (CI) 1.32–4.55], serum albumin <3.5 mg/dl (OR 1.76, 95%CI 1.05–2.94), MELD (model for end-stage liver disease) score >20 (OR 2.01, 95%CI 1.17–3.44), operation time >600 min (OR 1.81, 95%CI 1.07–3.06), warm ischemic time >40 min (OR 2.61, 95%CI 1.55–4.38), postreperfusion syndrome (OR 2.96, 95%CI 1.55–4.38), mean blood glucose during the day of surgery >150 mg/dl (OR 1.66, 95%CI 1.01–2.70), cryoprecipitate > 6 units (OR 4.96, 95%CI 2.84–8.64), blood loss/body weight >60 ml/kg (OR 4.05, 95%CI 2.28–7.21), and calcineurin inhibitor use without combined mycophenolate mofetil (OR 1.87, 95%CI 1.14–3.06). Our risk models performed better than did a previously reported score by Utsumi et al. in our study cohort. Doses of calcineurin inhibitor should be reduced by combined use of mycophenolate mofetil to decrease postoperative AKI. Prospective randomized trials are required to address whether artificial modification of hypoalbuminemia, hyperglycemia and postreperfusion syndrome would decrease postoperative AKI in LDLT.

Protein kinases participate in the contraction in response to levobupivacaine in the rat aorta.

Levobupivacaine is a long-acting amide local anesthetic that intrinsically produces vasoconstriction both in vivo and in vitro. Levobupivacaine increases intracellular calcium concentrations ([Ca(2+)](i)) in vascular smooth muscle cells. The goals of this in vitro study were to investigate whether levobupivacaine-induced contraction is associated with increased Ca(2+) sensitivity and to identify the protein kinases involved in mediating contraction in response to levobupivacaine in isolated rat aortic smooth muscle. The effect of levobupivacaine and potassium chloride (KCl) on the [Ca(2+)](i) and tension was measured simultaneously with acetoxymethyl ester of fura-2-loaded aortic strips. Cumulative levobupivacaine concentration-response curves were generated in the presence or absence of the following antagonists: GF 109203X; Y-27632; genistein; SP600125; PD 98059; and SB 203580. Levobupivacaine-induced protein kinase C (PKC), extracellular signal-regulated kinase (ERK), and c-Jun NH(2)-terminal kinase (JNK) phosphorylation and Rho-kinase (ROCK-2) membrane translocation were detected in rat aortic vascular smooth muscle cells using Western blotting. The slope of the [Ca(2+)](i)-tension curve for levobupivacaine was higher than that for KCl. Y-27632, GF 109203X, and SP600125 attenuated levobupivacaine-induced contraction in a concentration-dependent manner. Genistein, PD 98059, and SB 203580 attenuated levobupivacaine-induced contraction. Pretreatment with GF 109203X and Y-27632 inhibited levobupivacaine-induced PKC phosphorylation and Rho-kinase (ROCK-2) membrane translocation, respectively. Pretreatment with SP600125 or PD 98059 attenuated the levobupivacaine-induced phosphorylation of JNK and ERK, respectively. These results indicate that levobupivacaine-induced contraction involving an increase in myofilament Ca(2+) sensitivity involves the primary activation of Rho-kinase-, PKC-, and JNK-mediated pathways of rat aortic smooth muscle.

Dexmedetomidine-induced contraction of isolated rat aorta is dependent on extracellular calcium concentration

Background Dexmedetomidine is a highly selective α2-adrenoceptor agonist that is widely used for sedation and analgesia during the perioperative period. Intravenous administration of dexmedetomidine induces transient hypertension due to vasoconstriction via the activation of the α2-adrenoceptor on vascular smooth muscle. The goal of this in vitro study is to investigate the calcium-dependent mechanism underlying dexmedetomidine-induced contraction of isolated endothelium-denuded rat aorta. Methods Isolated endothelium-denuded rat thoracic aortic rings were suspended for isometric tension recording. Cumulative dexmedetomidine concentration-response curves were generated in the presence or absence of the following inhibitors: α2-adrenoceptor inhibitor rauwolscine; voltage-operated calcium channel blocker verapamil (5 × 10-7, 10-6 and 5 × 10-5 M); purported inositol 1,4,5-trisphosphate receptor blocker 2-aminoethoxydiphenylborate (5 × 10-6, 10-5 and 5 × 10-5 M); phospholipase C inhibitor U-73122 (10-6 and 3 × 10-6 M); and store-operated calcium channel inhibitor gadolinium chloride hexahydrate (Gd3+; 5 × 10-6 M). Dexmedetomidine concentration-response curves were also generated in low calcium concentrations (1 mM) and calcium-free Krebs solution. Results Rauwolscine, verapamil, and 2-aminoethoxydiphenylborate attenuated dexmedetomidine-induced contraction in a concentration-dependent manner. Low calcium concentrations attenuated dexmedetomidine-induced contraction, and calcium-free Krebs solution nearly abolished dexmedetomidine-induced contraction. However, U-73122 and Gd3+ had no effect on dexmedetomidine-induced contraction. Conclusions Taken together, these results suggest that dexmedetomidine-induced contraction is primarily dependent on extracellular calcium concentrations that contribute to calcium influx via voltage-operated calcium channels of isolated rat aortic smooth muscle. Dexmedetomidine-induced contraction is mediated by α2-adrenoceptor stimulation. Dexmedetomidine-induced contraction appears to be partially mediated by calcium release from the sarcoplasmic reticulum.

Systemic blockage of nitric oxide synthase by L-NAME increases left ventricular systolic pressure, which is not augmented further by Intralipid®.

Intravenous lipid emulsions (LEs) are effective in the treatment of toxicity associated with various drugs such as local anesthetics and other lipid soluble agents. The goals of this study were to examine the effect of LE on left ventricular hemodynamic variables and systemic blood pressure in an in vivo rat model, and to determine the associated cellular mechanism with a particular focus on nitric oxide. Two LEs (Intralipid® 20% and Lipofundin® MCT/LCT 20%) or normal saline were administered intravenously in an in vivo rat model following induction of anesthesia by intramuscular injection of tiletamine/zolazepam and xylazine. Left ventricular systolic pressure (LVSP), blood pressure, heart rate, maximum rate of intraventricular pressure increase, and maximum rate of intraventricular pressure decrease were measured before and after intravenous administration of various doses of LEs or normal saline to an in vivo rat with or without pretreatment with the non-specific nitric oxide synthase inhibitor Nω-nitro-L-arginine-methyl ester (L-NAME). Administration of Intralipid® (3 and 10 ml/kg) increased LVSP and decreased heart rate. Pretreatment with L-NAME (10 mg/kg) increased LSVP and decreased heart rate, whereas subsequent treatment with Intralipid® did not significantly alter LVSP. Intralipid® (10 ml/kg) increased mean blood pressure and decreased heart rate. The increase in LVSP induced by Lipofundin® MCT/LCT was greater than that induced by Intralipid®. Intralipid® (1%) did not significantly alter nitric oxide donor sodium nitroprusside-induced relaxation in endothelium-denuded rat aorta. Taken together, systemic blockage of nitric oxide synthase by L-NAME increases LVSP, which is not augmented further by intralipid®.

The effects of uterine artery embolization on ovarian reserve

OBJECTIVE To evaluate the effects of UAE for symptomatic uterine fibroids on ovarian reserve based on AMH. STUDY DESIGN This was a retrospective study conducted between March 2011 and October 2014. All women underwent UAE. At baseline and at the 3-month and 12-month follow-up visits, serum anti-Müllerian hormone (AMH), follicle stimulating hormone (FSH), luteinizing hormone (LH), and estradiol (E2) levels were assessed, and ovarian volume and antral follicle count (AFC) were evaluated in each patient. RESULTS There were no statistically significant differences in serum E2, LH, or FSH levels or in ovarian volume 3 or 12 months after UAE (P=0.8194, P=0.3976, P=0.4766, and P=0.6822, respectively). However, AMH and AFC were significantly different 3 and 12 months after the procedure (P=0.00, P=0.029 and P=0.00, P=0.00, respectively). AMH levels remained low after 12 months of follow-up compared to the expected AMH levels. A statistically significant recovery of serum AMH at 12 months compared to at 3 months in those <40 years of age (P=0.00), but not in those ≥40 years (P=0.837). CONCLUSIONS Ovarian reserve appears to be affected by UAE in premenopausal women. However, younger ovaries (according to biological ovarian age) exhibit a greater capacity for recovery after ovarian damage. Therefore, larger studies are needed for more conclusive results.

Association between recovery from Bell's palsy and body mass index

Although many factors have been found to be involved in recovery from Bells palsy, no study has investigated the association between recovery from Bells palsy and obesity. This study therefore evaluated the association between recovery from Bells palsy and body mass index (BMI).

Predictive Value of Intraoperative Thromboelastometry for the Risk of Perioperative Excessive Blood Loss in Infants and Children Undergoing Congenital Cardiac Surgery: A Retrospective Analysis

OBJECTIVE Laboratory hemostatic variables and parameters of rotational thromboelastometry (ROTEM) were evaluated for their ability to predict perioperative excessive blood loss (PEBL) after congenital cardiac surgery. DESIGN Retrospective and observational. SETTING Single, large university hospital. PARTICIPANTS The study comprised 119 children younger than 10 years old undergoing congenital cardiac surgery with cardiopulmonary bypass (CPB). MEASUREMENTS AND MAIN RESULTS Intraoperative excessive blood loss was defined as estimated blood loss≥50% of estimated blood volume (EBV). Postoperative excessive blood loss was defined as measured postoperative chest tube and Jackson-Pratt drainage≥30% of EBV over 12 hours or≥50% of EBV over 24 hours in the intensive care unit. PEBL was defined as either intraoperative or postoperative excessive blood loss. External temogram (EXTEM) and fibrinogen temogram (FIBTEM) were analyzed before and after CPB with ROTEM and laboratory hemostatic variables. Multivariate logistic regression was performed. Incidence of PEBL was 19.3% (n = 23). Independent risk factors for PEBL were CPB time>120 minutes, post-CPB FIBTEM alpha-angle, clot firmness after 10 minutes<5 mm, post-CPB EXTEM alpha-angle, clot firmness after 10 minutes<30 mm, and post-CPB EXTEM maximal lysis>20%. Laboratory hemostatic variables were not significant in multivariate analysis. The risk prediction model was developed from the results of multivariate analysis. The area under the receiver operating characteristic curve was 0.94 (95% confidence interval: 0.90-0.99). CONCLUSIONS Post-CPB ROTEM may be useful for predicting both intraoperative and postoperative excessive blood loss in congenital cardiac surgery. This study provided an accurate prediction model for PEBL and supported intraoperative transfusion guidance using post-CPB FIBTEM-A10 and EXTEM-A10.

Comparative Analysis of the Combined Therapeutic Effects of Lipoprostaglandin E 1 on Sudden Idiopathic Sensorineural Hearing Loss

Background and Objectives Viral and vascular disorders are considered to be a major cause of idiopathic sudden sensorineural hearing loss (ISSNHL). Lipoprostaglandin E1 (lipo-PGE1) has vasodilating activity and has been used to treat ISSNHL. The purpose of this study was to determine the specific therapeutic effects of lipo-PGE1 and compare them to other treatment modalities for ISSNHL. Subjects and Methods The study group had 1,052 patients diagnosed with ISSNHL. All were treated with steroid, carbogen inhalation, stellate ganglion block (SGB), or PGE1. The CP group (steroid, carbogen inhalation, and PGE1 injection; 288 patients) was treated with lipo-PGE1 and carbogen inhalation, the CS group (steroid, carbogen inhalation, and stellate ganglion block; 232 patients) with steroid, carbogen inhalation, and SGB, the C group (steroid and carbogen inhalation; 284 patients) with steroid and carbogen, and the control group (steroid only; 248 patients) with steroid only. Patients in the groups receiving lipo-PGE1 received a continuous infusion of 10 µL lipo-PGE1. Results The overall recovery rate after treatment was 52.2%, and recovery rates by group were 67.7% in the CP group, 54.3% in the CS group, 52.1% in the C group, and 32.2% in the control group. Therefore, the therapeutic results in groups treated with lipo-PGE1 were better than results in other groups. The difference was statistically significant. Conclusions The study results suggested that the CP group received effective treatment modalities for ISSNHL. The combined therapy of lipo-PGE1 with carbogen inhalation in patients with ISSNHL was more beneficial than other treatment modalities.

Association of Metabolic Syndrome With Sudden Sensorineural Hearing Loss

Importance Each of the 5 diagnostic criteria or factors of metabolic syndrome—hyperglycemia or type 2 diabetes, hypertension, obesity, elevated triglyceride levels, and decreased high-density lipoprotein cholesterol level—is associated with the pathophysiologic features of sudden sensorineural hearing loss (SSNHL). Little is known, however, about the association of metabolic syndrome, defined as the presence of at least 3 of these factors, with the prognosis of SSNHL. Objective To evaluate the association of metabolic syndrome with the rate of recovery from SSNHL. Design, Setting, and Participants This retrospective medical record review of 124 patients treated for SSNHL at a single tertiary university hospital was performed from June 1, 2014, through May 31, 2016. Medical records were reviewed for demographic and clinical characteristics and audiologic variables. Exposure Sudden sensorineural hearing loss. Main Outcomes and Measures Correlation among demographic and clinical characteristics, audiologic results, and prognosis. Results Of the total 124 patients (52 men [41.9%]; 72 women [58.1%]; mean [SD] age, 56.0 [14.6] years), 70 had metabolic syndrome and 54 did not. Rates of type 2 diabetes (36 [51.4%] vs 6 [11.1%]; mean difference [MD], 40.3%; 95% CI, 24.4%-53.1%), hypertension (46 [65.7%] vs 9 [16.7%]; MD, 49.1%; 95% CI, 32.3%-61.7%), and obesity (47 [67.1%] vs 6 [11.1%]; MD%, 56.0; 95% CI, 40.0%-67.5%) and mean (SD) concentrations of triglycerides (192.9 [159.7] vs 133.4 [116.6] mg/dL; MD, 59.4 mg/dL; 95% CI, 53.0-65.9 mg/dL) were significantly higher and mean (SD) concentrations of high-density lipoprotein cholesterol (45.8 [9.4] vs 62.6 [17.7] mg/dL; MD, 16.8 mg/dL; 95% CI, 16.1-17.4 mg/dL) were significantly lower in the group with metabolic syndrome than in the group without metabolic syndrome. Mean (SD) pure-tone audiometry thresholds were similar at baseline in the groups with and without metabolic syndrome (65.0 [24.2] vs 60.8 [24.2] dB; MD, 4.3 dB; 95% CI, 3.2-5.4 dB), but recovery rates after treatment were significantly lower in the group with metabolic syndrome (16 [22.9%] vs 23 [42.6%]; MD, −19.7%; 95% CI, −35.4% to −3.2%). No differences were found in the 5 factors among patients with metabolic syndrome who did and did not recover. Level of hearing loss was higher in patients with than without metabolic syndrome, but the difference was not statistically significant. Audiogram patterns also differed but not significantly. Hearing recovery rates were similar in patients with 3 factors of metabolic syndrome and those with none but differed significantly between patients with 4 or more factors and those without metabolic syndrome (4 [19.0%] vs 27 [50.0%]; MD, −31.0%; 95% CI, −48.1% to −6.4%). Conclusions and Relevance The rate of recovery from SSNHL was lower among patients with metabolic syndrome than among those without metabolic syndrome, and prognosis was poorer in patients with 4 or more diagnostic factors of the metabolic syndrome.