Clinical Focus


  • Anesthesia

Academic Appointments


Administrative Appointments


  • Director, Urology rotation, Department of Anesthesiology, Pain and Perioperative Medicine (2012 - Present)

Professional Education


  • Dr. med., University of Technology, Dresden, Germany, Depth of anesthesia monitoring and propofol (2005)
  • Residency, University of Technology, Dresden, Germany, Anesthesiology (2003)
  • Residency: Heart Center Dresden (2000) Germany
  • Medical Education: Philipps University Marburg (1997) Germany

Community and International Work


  • Medical mission, Phnom Penh, Cambodia

    Topic

    Children

    Partnering Organization(s)

    Smile Cambodia

    Populations Served

    Children

    Location

    International

    Ongoing Project

    No

    Opportunities for Student Involvement

    No

  • Medical mission, Imo State, Nigeria

    Topic

    Anesthesia in rural Nigeria

    Populations Served

    Children and adults

    Location

    International

    Ongoing Project

    No

    Opportunities for Student Involvement

    No

All Publications


  • The effect of hyperoxia on ventilation during recovery from general anesthesia: A randomized pilot study for a parallel randomized controlled trial. Journal of clinical anesthesia Doufas, A. G., Tian, L., Kutscher, S., Finnsson, E., Ágústsson, J. S., Chung, B. I., Panousis, P. 2022; 83: 110982

    Abstract

    While supplemental O2 inhalation corrects hypoxemia, its effect on post-anesthesia ventilation remains unknown. This pilot trial tested the hypothesis that hyperoxia increases the time spent with a transcutaneous PCO2 (TcPCO2) > 45 mmHg, compared with standard O2 supplementation.Single-blinded, parallel two-arm randomized pilot trial.University hospital.20 patients undergoing robotic-assisted laparoscopic nephrectomy.After institutional approval and informed consent, patients were randomized to receive O2 titrated to arterial saturation (SpO2): 90-94% (Conservative O2, N =10), or to SpO2 > 96% (Liberal O2, N = 10) for up to 90 min after anesthesia. Continuous TcPCO2, respiratory inductance plethysmography (RIP), and SpO2, were recorded. We calculated the percentage of time at TcPCO2 > 45 mmHg for each patient and compared the two groups using analysis of covariance, adjusting for sex, age, and body mass index. We also estimated the sample size required to detect the between-group difference observed in this pilot trial. RIP signals were used to calculate apnea/hypopnea index (AHI), which was then compared between two groups.The mean percentage of time with a TcPCO2 > 45 mmHg was 80.6% for the Conservative O2 (N=9) and 61.2% for the Liberal O2 (N=10) group [between-group difference of 19.4% (95% CI: -18.7% to 57.6%), P = 0.140]. With an observed effect size of 0.73, we estimated that 30 participants per group are required, to demonstrate this difference with a power of 80% at a two-sided alpha of 5%. Means SpO2 were 94.5% and 99.9% for the Conservative O2 and the Liberal O2 groups, respectively. AHI was significantly higher in the Conservative O2, compared with the Liberal O2 group (median AHI: 16 vs. 3; P = 0.0014).Hyperoxia in the post-anesthesia period reduced the time spent at TcPCO2 > 45 mmHg and significantly decreased AHI, while mean SpO2 ranged inside the a priori defined limits.ClinicalTrials.gov identifier: NCT04723433.

    View details for DOI 10.1016/j.jclinane.2022.110982

    View details for PubMedID 36265267

  • Syndrome of inappropriate secretion of antidiuretic hormone following high dose rate brachytherapy for prostate cancer: a case report. BMC urology Ayoola, A., Sodji, Q. H., Chin, S., Panousis, P., Bagshaw, H. P., Buyyounouski, M. K. 2022; 22 (1): 32

    Abstract

    The syndrome of inappropriate secretion of antidiuretic hormone is a disorder characterized by the excess release of antidiuretic hormone and can result in hyponatremia. If managed inappropriately, severe hyponatremia can cause seizures, cerebral edema, and even death. There are various known causes of this inappropriate release of antidiuretic hormone, including malignancy, CNS disorders, and disturbances in the hypothalamic-pituitary-renal axis. However, reports of syndrome of inappropriate secretion of antidiuretic hormone after brachytherapy for prostate cancer are exceedingly rare.We report a case of symptomatic hyponatremia secondary to the inappropriate secretion of antidiuretic hormone after prostate high-dose rate brachytherapy under general anesthesia in a patient with adenocarcinoma of the prostate.In rare instances, inappropriate secretion of antidiuretic hormone can occur after high-dose rate brachytherapy for prostate cancer. The cause is likely multifactorial, involving pain or discomfort ensuing from the surgical procedure, the general anesthesia or intraoperative drugs administered. However, due to the potential severity of the side effects, timely diagnosis is crucial to ensure prompt, and effective management.

    View details for DOI 10.1186/s12894-022-00984-y

    View details for PubMedID 35272646

  • Insomnia From Drug Treatments: Evidence From Meta-analyses of Randomized Trials and Concordance With Prescribing Information. Mayo Clinic proceedings Doufas, A. G., Panagiotou, O. A., Panousis, P., Wong, S. S., Ioannidis, J. P. 2017; 92 (1): 72-87

    Abstract

    To determine whether drugs used to treat diverse conditions cause insomnia symptoms and whether their prescription information is concordant with this evidence.We conducted a survey of meta-analyses (Cochrane Database of Systematic Reviews) and comparisons with package inserts compiled in the Physicians' Desk Reference (PDR). We identified randomized controlled trials (RCTs) in which any drug had been evaluated vs placebo and sleep had been assessed. We collectively referred to insomnia-related outcomes as sleep disturbance. We also searched the PDR to identify any insomnia symptoms listed for drugs with RCT evidence available.Seventy-four Cochrane systematic reviews corresponding to 274 RCTs assessed 88 drugs in 27 different conditions, providing evidence on 109 drug-condition pairs. Of these 88 drugs, 5 decreased sleep problems and 19 increased sleep problems; 64 drugs had no nominally statistically significant effect on sleep. Acetylcholinesterase inhibitors, dopamine agonists, and selective serotonin reuptake inhibitors were the drug classes most importantly associated with sleep disturbance. Of 35 drugs that included disturbed sleep as an adverse effect in the PDR, only 14 had RCT evidence supporting such effect, and 2 had evidence of increasing and decreasing sleep problems in RCTs, although this was not shown in the PDR. We identified weak concordance between the PDR and RCTs (weighted κ=0.31; P<.001).The RCTs offer substantial evidence about the common effects of drugs on the risk of sleep disturbance; currently, prescription information only partially agrees with the available randomized evidence.

    View details for DOI 10.1016/j.mayocp.2016.09.005

    View details for PubMedID 27842706

  • Epidural Ropivacaine Concentrations for Intraoperative Analgesia During Major Upper Abdominal Surgery: A Prospective, Randomized, Double-Blinded, Placebo-Controlled Study ANESTHESIA AND ANALGESIA Panousis, P., Heller, A. R., Koch, T., Litz, R. J. 2009; 108 (6): 1971-1976

    Abstract

    The postoperative beneficial effects of thoracic epidural analgesia (TEA) within various clinical pathways are well documented. However, intraoperative data are lacking on the effect of different epidurally administered concentrations of local anesthetics on inhaled anesthetic, fluid and vasopressor requirement, and hemodynamic changes. We performed this study among patients undergoing major upper abdominal surgery under combined TEA and general anesthesia.Forty-five patients undergoing major upper abdominal surgery were randomly assigned to one of three treatment groups receiving intraoperative TEA with either 10 mL of 0.5% (Group 1) or 0.2% (Group 2) ropivacaine (both with 0.5 microg/mL sufentanil supplement), or 10 mL saline (Group 3) every 60 min. Anesthesia was maintained with desflurane in nitrous oxide (60%) initiated at an age-adapted 1 minimum alveolar concentration (MAC) until incision. Desflurane administration was then titrated to maintain an anesthetic level between 50 and 55, as assessed by continuous Bispectral Index monitoring and the common clinical signs (PRST score). Lack of intraoperative analgesia, as defined by an increase in pulse rate, sweating, and tearing (PRST) score >2 or an increase of mean arterial blood pressure (MAP) >20% of baseline, was treated by readjusting the end-tidal concentration of desflurane toward 1 MAC, and above this level by additional rescue i.v. remifentanil infusion. Hypotension, as defined as a decrease in MAP >20% of baseline, was treated by reducing the end-tidal desflurane concentration to a Bispectral Index level of 50-55 and below that with crystalloid or norepinephrine infusion, depending on central venous pressure.End-tidal desflurane concentration could be significantly reduced in Group 1 to 0.7 +/- 0.1 MAC (P < 0.001) and to 0.8 +/- 0.1 MAC (P < 0.001) in Group 2, but not in Group 3. Significant hypotension occurred within 20 min in all patients of Groups 1 and 2 (MAP from 80 +/- 10 to 56 +/- 5) (Group 1), 78 +/- 18 to 58 +/- 7 mm Hg (Group 2), P < 0.01, whereas MAP remained unchanged in Group 3 (74 +/- 12 to 83 +/- 15 mm Hg, P = 0.42). Heart rate did not change significantly over time within any of the groups. Furthermore, groups did not differ significantly regarding i.v. fluid and norepinephrine requirement. Patients in Group 3 received more remifentanil throughout the surgical procedure (7.2 +/- 4.9 mg x kg(-1) x h(-1)) when compared with Group 2 (1.6 +/- 2.2 mg x kg(-1) x h(-1)), P < 0.01. Remifentanil infusion among patients receiving ropivacaine 0.5% was not necessary at any time.Epidural administration of 0.5% ropivacaine leads to a more pronounced sparing effect on desflurane concentration for an adequate anesthetic depth when compared with a 0.2% concentration of ropivacaine at comparable levels of vasopressor support and i.v. fluid requirement.

    View details for DOI 10.1213/ane.0b013e3181a2a301

    View details for Web of Science ID 000266285500044

    View details for PubMedID 19448234