Skip to main content
Hauptrubriken
CME Facharzt-Training Webinare Zeitschriften Bücher e.Medpedia Podcast
Service
Jobbörse Info & Hilfe
Fachgebiete
Anästhesiologie Allgemeinmedizin Arbeitsmedizin Augenheilkunde Chirurgie Dermatologie Gynäkologie und Geburtshilfe HNO Innere Medizin Kardiologie Neurologie Onkologie und Hämatologie Orthopädie und Unfallchirurgie Pädiatrie Pathologie Psychiatrie Radiologie Rechtsmedizin Urologie Zahnmedizin
Themen
Klimawandel und Gesundheit Neues aus dem Markt COVID-19 Praxis und Beruf Seltene Erkrankungen GOÄ & EBM Panorama
Sammlungen
Kasuistiken Algorithmen & Infografiken Blickdiagnosen Arthropedia FlapFinder (für Dermatochirurgen) Videos Kongressberichterstattung Medizin für Apothekerinnen und Apotheker Für Ärztinnen und Ärzte in Weiterbildung Für Medizinstudierende
Erweiterte Suche
Anmelden
nach oben
Obesity Surgery
Erschienen in: Obesity Surgery 6/2012

01.06.2012 | Review

Bariatric Surgery and the Central Nervous System

verfasst von: Raghavendra S. Rao

Erschienen in: Obesity Surgery | Ausgabe 6/2012

Einloggen, um Zugang zu erhalten

Abstract

Bariatric procedures are now known to have an effect on hunger as well as on metabolism. The role of central nervous pathways in causing these effects after bariatric surgery is now being elucidated. A brief overview of these pathways has been presented for the sake of bariatric surgeons. A PubMed search was made using various search phrases to retrieve all original articles concerning the effect of bariatric surgery on the neural pathways. The mechanisms regulating the food intake and energy expenditure can be broadly divided into homeostatic and hedonic systems. The effect of bariatric surgery on the homeostatic system in animal models is not clear. A decrease in preference for sweet taste and high calorie foods has been demonstrated in animal models. The effect of bariatric surgery on the hedonic system in humans has been consistent with decreased activation of the hedonic system being demonstrated by functional MRI and decreased preference for intake of high energy foods also being observed post-surgery. The effect of bariatric surgery on dopamine signaling, which is involved in the hedonic system, is however not clear. Functional MRI studies have also demonstrated increased activation of the hypothalamus after surgery. Various studies utilizing questionnaires have demonstrated increased satiety and decreased hunger after bariatric surgery.
Literatur
1.
Hetherington AW, Ranson SW. Hypothalamic lesions and adiposity in the rat. The Anatomical Record. 1940;78:149–72.
2.
Dhillon H, Zigman JM, Ye C, et al. Leptin directly activates SF1 neurons in the VMH, and this action by leptin is required for normal body-weight homeostasis. Neuron. 2006;49:191–203.PubMedCrossRef
3.
Balthasar N. Genetic dissection of neuronal pathways controlling energy homeostasis. Obesity (Silver Spring). 2006;14 Suppl 5:222S–7S.CrossRef
4.
Nestler EJ. Molecular basis of long-term plasticity underlying addiction. Nat Rev Neurosci. 2001;2:119–28.PubMedCrossRef
5.
Barrot M, Olivier JD, Perrotti LI, et al. CREB activity in the nucleus accumbens shell controls gating of behavioral responses to emotional stimuli. Proc Natl Acad Sci U S A. 2002;99:11435–40.PubMedCrossRef
6.
7.
Stoeckel LE, Weller RE, Cook 3rd EW, et al. Widespread reward-system activation in obese women in response to pictures of high-calorie foods. NeuroImage. 2008;41:636–47.PubMedCrossRef
8.
Stice E, Spoor S, Bohon C, et al. Relation between obesity and blunted striatal response to food is moderated by TaqIA A1 allele. Science. 2008;322(5900):449–52.PubMedCrossRef
9.
Rothemund Y, Preuschhof C, Bohner G, et al. Differential activation of the dorsal striatum by high-calorie visual food stimuli in obese individuals. NeuroImage. 2007;37:410–21.PubMedCrossRef
10.
Rosenbaum M, Sy M, Pavlovich K, et al. Leptin reverses weight loss-induced changes in regional neural activity responses to visual food stimuli. J Clin Invest. 2008;118:2583–91.PubMed
11.
Dzaja A, Dalal MA, Himmerich H, et al. Sleep enhances nocturnal plasma ghrelin levels in healthy subjects. Am J Physiol Endocrinol Metab. 2004;286:E963–7.PubMedCrossRef
12.
Shiiya T, Nakazato M, Mizuta M, et al. Plasma ghrelin levels in lean and obese humans and the effect of glucose on ghrelin secretion. J Clin Endocrinol Metab. 2002;87:240–4.PubMedCrossRef
13.
Yildiz BO, Suchard MA, Wong ML, et al. Alterations in the dynamics of circulating ghrelin, adiponectin, and leptin in human obesity. Proc Natl Acad Sci U S A. 2004;101:10434–9.PubMedCrossRef
14.
Date Y, Murakami N, Toshinai K, et al. The role of the gastric afferent vagal nerve in ghrelin-induced feeding and growth hormone secretion in rats. Gastroenterology. 2002;123:1120–8.PubMedCrossRef
15.
Kojima M, Hosoda H, Date Y, et al. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999;402:656–60.PubMedCrossRef
16.
Cowley MA, Smith RG, Diano S, et al. The distribution and mechanism of action of ghrelin in the CNS demonstrates a novel hypothalamic circuit regulating energy homeostasis. Neuron. 2003;37:649–61.PubMedCrossRef
17.
Karamanakos SN, Vagenas K, Kalfarentzos F, et al. Weight loss, appetite suppression, and changes in fasting and postprandial ghrelin and peptide-YY levels after Roux-en-Y gastric bypass and sleeve gastrectomy: a prospective, double blind study. Ann Surg. 2008;247:401–7.PubMedCrossRef
18.
Adrian TE, Ferri GL, Bacarese-Hamilton AJ, et al. Human distribution and release of a putative new gut hormone, peptide YY. Gastroenterology. 1985;89:1070–7.PubMed
19.
Di Francesco V, Zamboni M, Dioli A, et al. Delayed postprandial gastric emptying and impaired gallbladder contraction together with elevated cholecystokinin and peptide YY serum levels sustain satiety and inhibit hunger in healthy elderly persons. J Gerontol A Biol Sci Med Sci. 2005;60:1581–5.PubMedCrossRef
20.
Batterham RL, Cowley MA, Small CJ, et al. Gut hormone PYY(3–36) physiologically inhibits food intake. Nature. 2002;418:650–4.PubMedCrossRef
21.
Acuna-Goycolea C, van den Pol AN. Peptide YY(3–36) inhibits both anorexigenic proopiomelanocortin and orexigenic neuropeptide Y neurons: implications for hypothalamic regulation of energy homeostasis. J Neurosci. 2005;25:10510–9.PubMedCrossRef
22.
Korner J, Inabnet W, Febres G, et al. Prospective study of gut hormone and metabolic changes after adjustable gastric banding and Roux-en-Y gastric bypass. Int J Obes (Lond). 2009;33:786–95.CrossRef
23.
Peterli R, Wolnerhanssen B, Peters T, et al. Improvement in glucose metabolism after bariatric surgery: comparison of laparoscopic Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy: a prospective randomized trial. Ann Surg. 2009;250:234–41.PubMedCrossRef
24.
Hedberg J, Hedenstrom H, Karlsson FA, et al. Gastric emptying and postprandial PYY response after biliopancreatic diversion with duodenal switch. Obes Surg. 2011;21:609–15.PubMedCrossRef
25.
Plum L, Ahmed L, Febres G, et al. Comparison of glucostatic parameters after hypocaloric diet or bariatric surgery and equivalent weight loss. Obesity (Silver Spring). 2011;19:2149–57.CrossRef
26.
Chandarana K, Gelegen C, Karra E, et al. Diet and gastrointestinal bypass-induced weight loss: the roles of ghrelin and peptide YY. Diabetes. 2011;60:810–8.PubMedCrossRef
27.
le Roux CW, Aylwin SJ, Batterham RL, et al. Gut hormone profiles following bariatric surgery favor an anorectic state, facilitate weight loss, and improve metabolic parameters. Ann Surg. 2006;243:108–14.PubMedCrossRef
28.
le Roux CW, Welbourn R, Werling M, et al. Gut hormones as mediators of appetite and weight loss after Roux-en-Y gastric bypass. Ann Surg. 2007;246:780–5.PubMedCrossRef
29.
Fekete C, Singru PS, Sanchez E, et al. Differential effects of central leptin, insulin, or glucose administration during fasting on the hypothalamic–pituitary–thyroid axis and feeding-related neurons in the arcuate nucleus. Endocrinology. 2006;147:520–9.PubMedCrossRef
30.
Gavrila A, Chan JL, Miller LC, et al. Circulating melanin-concentrating hormone, agouti-related protein, and alpha-melanocyte-stimulating hormone levels in relation to body composition: alterations in response to food deprivation and recombinant human leptin administration. J Clin Endocrinol Metab. 2005;90:1047–54.PubMedCrossRef
31.
Singru PS, Sanchez E, Fekete C, et al. Importance of melanocortin signaling in refeeding-induced neuronal activation and satiety. Endocrinology. 2007;148:638–46.PubMedCrossRef
32.
Kelesidis T, Kelesidis I, Chou S, et al. Narrative review: the role of leptin in human physiology: emerging clinical applications. Ann Intern Med. 2010;152:93–100.PubMed
33.
Buettner C, Muse ED, Cheng A, et al. Leptin controls adipose tissue lipogenesis via central, STAT3-independent mechanisms. Nat Med. 2008;14:667–75.PubMedCrossRef
34.
Minokoshi Y, Haque MS, Shimazu T. Microinjection of leptin into the ventromedial hypothalamus increases glucose uptake in peripheral tissues in rats. Diabetes. 1999;48:287–91.PubMedCrossRef
35.
Pinto S, Roseberry AG, Liu H, et al. Rapid rewiring of arcuate nucleus feeding circuits by leptin. Science. 2004;304:110–5.PubMedCrossRef
36.
Caro JF, Kolaczynski JW, Nyce MR, et al. Decreased cerebrospinal-fluid/serum leptin ratio in obesity: a possible mechanism for leptin resistance. Lancet. 1996;348:159–61.PubMedCrossRef
37.
Meguid MM, Glade MJ, Middleton FA. Weight regain after Roux-en-Y: a significant 20 % complication related to PYY. Nutrition. 2008;24:832–42.PubMedCrossRef
38.
Spranger J, Verma S, Gohring I, et al. Adiponectin does not cross the blood–brain barrier but modifies cytokine expression of brain endothelial cells. Diabetes. 2006;55:141–7.PubMedCrossRef
39.
Donahey JC, van Dijk G, Woods SC, et al. Intraventricular GLP-1 reduces short- but not long-term food intake or body weight in lean and obese rats. Brain Res. 1998;779:75–83.PubMedCrossRef
40.
Baraboi ED, St-Pierre DH, Shooner J, et al. Brain activation following peripheral administration of the GLP-1 receptor agonist exendin-4. Am J Physiol Regul Integr Comp Physiol. 2011;301:R1011–24.PubMedCrossRef
41.
Knauf C, Cani PD, Kim DH, et al. Role of central nervous system glucagon-like peptide-1 receptors in enteric glucose sensing. Diabetes. 2008;57:2603–12.PubMedCrossRef
42.
Burmeister MA, Ferre T, Ayala JE, et al. Acute activation of central GLP-1 receptors enhances hepatic insulin action and insulin secretion in high-fat-fed, insulin resistant mice. Am J Physiol Endocrinol Metab. 2012;302(3):E334–43.PubMedCrossRef
43.
Ma X, Bruning J, Ashcroft FM. Glucagon-like peptide 1 stimulates hypothalamic proopiomelanocortin neurons. J Neurosci. 2007;27:7125–9.PubMedCrossRef
44.
Boschmann M, Engeli S, Dobberstein K, et al. Dipeptidyl-peptidase-IV inhibition augments postprandial lipid mobilization and oxidation in type 2 diabetic patients. J Clin Endocrinol Metab. 2009;94:846–52.PubMedCrossRef
45.
Elias CF, Kelly JF, Lee CE, et al. Chemical characterization of leptin-activated neurons in the rat brain. J Comp Neurol. 2000;423:261–81.PubMedCrossRef
46.
Valverde I, Puente J, Martin-Duce A, et al. Changes in glucagon-like peptide-1 (GLP-1) secretion after biliopancreatic diversion or vertical banded gastroplasty in obese subjects. Obes Surg. 2005;15:387–97.PubMedCrossRef
47.
Hommel JD, Trinko R, Sears RM, et al. Leptin receptor signaling in midbrain dopamine neurons regulates feeding. Neuron. 2006;51:801–10.PubMedCrossRef
48.
Farooqi IS, Bullmore E, Keogh J, et al. Leptin regulates striatal regions and human eating behavior. Science. 2007;317:1355.PubMedCrossRef
49.
Abizaid A, Liu ZW, Andrews ZB, et al. Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite. J Clin Invest. 2006;116:3229–39.PubMedCrossRef
50.
Diano S, Farr SA, Benoit SC, et al. Ghrelin controls hippocampal spine synapse density and memory performance. Nat Neurosci. 2006;9:381–8.PubMedCrossRef
51.
Jerlhag E, Egecioglu E, Dickson SL, et al. Ghrelin administration into tegmental areas stimulates locomotor activity and increases extracellular concentration of dopamine in the nucleus accumbens. Addict Biol. 2007;12:6–16.PubMedCrossRef
52.
Naleid AM, Grace MK, Cummings DE, et al. Ghrelin induces feeding in the mesolimbic reward pathway between the ventral tegmental area and the nucleus accumbens. Peptides. 2005;26:2274–9.PubMedCrossRef
53.
Malik S, McGlone F, Bedrossian D, et al. Ghrelin modulates brain activity in areas that control appetitive behavior. Cell Metab. 2008;7:400–9.PubMedCrossRef
54.
Bueter M, le Roux CW. Gastrointestinal hormones, energy balance and bariatric surgery. Int J Obes (Lond). 2011;35 Suppl 3:S35–9.CrossRef
55.
Rao RS, Rao V, Kini S. Animal models in bariatric surgery—a review of the surgical techniques and postsurgical physiology. Obes Surg. 2010;20:1293–305.PubMedCrossRef
56.
Romanova IV, Ramos EJ, Xu Y, et al. Neurobiologic changes in the hypothalamus associated with weight loss after gastric bypass. J Am Coll Surg. 2004;199:887–95.PubMedCrossRef
57.
Nadreau E, Baraboi ED, Samson P, et al. Effects of the biliopancreatic diversion on energy balance in the rat. Int J Obes (Lond). 2006;30:419–29.CrossRef
58.
Wang Y, Liu J. Plasma ghrelin modulation in gastric band operation and sleeve gastrectomy. Obes Surg. 2009;19:357–62.PubMedCrossRef
59.
Li JV, Ashrafian H, Bueter M, et al. Metabolic surgery profoundly influences gut microbial-host metabolic cross-talk. Gut. 2011;60:1214–23.PubMedCrossRef
60.
Sonoda EY, Gomes da Silva S, Arida RM, et al. Hippocampal plasticity in rats submitted to a gastric restrictive procedure. Nutr Neurosci. 2011;14:181–5.PubMedCrossRef
61.
Shin AC, Zheng H, Pistell PJ, et al. Roux-en-Y gastric bypass surgery changes food reward in rats. Int J Obes (Lond). 2011;35:642–51.CrossRef
62.
Dunn JP, Cowan RL, Volkow ND, et al. Decreased dopamine type 2 receptor availability after bariatric surgery: preliminary findings. Brain Res. 2010;1350:123–30.PubMedCrossRef
63.
Steele KE, Prokopowicz GP, Schweitzer MA, et al. Alterations of central dopamine receptors before and after gastric bypass surgery. Obes Surg. 2010;20:369–74.PubMedCrossRef
64.
Bruce JM, Hancock L, Bruce A, et al. Changes in brain activation to food pictures after adjustable gastric banding. Surg Obes Relat Dis. 2011.
65.
Ochner CN, Kwok Y, Conceicao E, et al. Selective reduction in neural responses to high calorie foods following gastric bypass surgery. Ann Surg. 2011;253:502–7.PubMedCrossRef
66.
van de Sande-Lee S, Pereira FR, Cintra DE, et al. Partial reversibility of hypothalamic dysfunction and changes in brain activity after body mass reduction in obese subjects. Diabetes. 2011;60:1699–704.PubMedCrossRef
67.
Halmi KA, Mason E, Falk JR, et al. Appetitive behavior after gastric bypass for obesity. Int J Obes. 1981;5:457–64.PubMed
68.
Thomas JR, Marcus E. High and low fat food selection with reported frequency intolerance following Roux-en-Y gastric bypass. Obes Surg. 2008;18:282–7.PubMedCrossRef
69.
Brown EK, Settle EA, Van Rij AM. Food intake patterns of gastric bypass patients. J Am Diet Assoc. 1982;80:437–43.PubMed
70.
Kenler HA, Brolin RE, Cody RP. Changes in eating behavior after horizontal gastroplasty and Roux-en-Y gastric bypass. Am J Clin Nutr. 1990;52:87–92.PubMed
71.
Olbers T, Bjorkman S, Lindroos A, et al. Body composition, dietary intake, and energy expenditure after laparoscopic Roux-en-Y gastric bypass and laparoscopic vertical banded gastroplasty: a randomized clinical trial. Ann Surg. 2006;244:715–22.PubMedCrossRef
72.
Scruggs DM, Buffington C, Cowan Jr GS. Taste acuity of the morbidly obese before and after gastric bypass surgery. Obes Surg. 1994;4:24–8.PubMedCrossRef
73.
Burge JC, Schaumburg JZ, Choban PS, et al. Changes in patients' taste acuity after Roux-en-Y gastric bypass for clinically severe obesity. J Am Diet Assoc. 1995;95:666–70.PubMedCrossRef
74.
Shimura T, Imaoka H, Okazaki Y, et al. Involvement of the mesolimbic system in palatability-induced ingestion. Chem Senses. 2005;30 Suppl 1:i188–9.PubMedCrossRef
75.
Schultes B, Ernst B, Wilms B, et al. Hedonic hunger is increased in severely obese patients and is reduced after gastric bypass surgery. Am J Clin Nutr. 2010;92:277–83.PubMedCrossRef
76.
Batterham RL, Ffytche DH, Rosenthal JM, et al. PYY modulation of cortical and hypothalamic brain areas predicts feeding behaviour in humans. Nature. 2007;450:106–9.PubMedCrossRef
77.
Thirlby RC, Bahiraei F, Randall J, et al. Effect of Roux-en-Y gastric bypass on satiety and food likes: the role of genetics. J Gastrointest Surg. 2006;10:270–7.PubMedCrossRef
78.
Kalarchian MA, Wilson GT, Brolin RE, et al. Effects of bariatric surgery on binge eating and related psychopathology. Eat Weight Disord. 1999;4:1–5.PubMed
79.
80.
Morrow J, Gluck M, Lorence M, et al. Night eating status and influence on body weight, body image, hunger, and cortisol pre- and post-Roux-en-Y gastric bypass (RYGB) surgery. Eat Weight Disord. 2008;13:e96–9.PubMed
81.
Burgmer R, Grigutsch K, Zipfel S, et al. The influence of eating behavior and eating pathology on weight loss after gastric restriction operations. Obes Surg. 2005;15:684–91.PubMedCrossRef
82.
Bueter M, Miras AD, Chichger H, et al. Alterations of sucrose preference after Roux-en-Y gastric bypass. Physiol Behav. 2011;104:709–21.PubMedCrossRef
83.
Tichansky DS, Glatt AR, Madan AK, et al. Decrease in sweet taste in rats after gastric bypass surgery. Surg Endosc. 2011;25:1176–81.PubMedCrossRef
84.
Hajnal A, Kovacs P, Ahmed T, et al. Gastric bypass surgery alters behavioral and neural taste functions for sweet taste in obese rats. Am J Physiol Gastrointest Liver Physiol. 2010;299:G967–79.PubMedCrossRef
85.
Mathes CM, Bueter M, Smith KR, et al. Roux-en-Y gastric bypass in rats increases sucrose taste-related motivated behavior independent of pharmacological GLP-1-receptor modulation. Am J Physiol Regul Integr Comp Physiol. 2012;302(6):R751–67.PubMedCrossRef
86.
le Roux CW, Bueter M, Theis N, et al. Gastric bypass reduces fat intake and preference. Am J Physiol Regul Integr Comp Physiol. 2011;301:R1057–66.PubMedCrossRef
Metadaten
Titel
Bariatric Surgery and the Central Nervous System
verfasst von
Raghavendra S. Rao
Publikationsdatum
01.06.2012
Verlag
Springer-Verlag
Erschienen in
Obesity Surgery / Ausgabe 6/2012
Print ISSN: 0960-8923
Elektronische ISSN: 1708-0428
DOI
https://doi.org/10.1007/s11695-012-0649-5

Weitere Artikel der Ausgabe 6/2012

Obesity Surgery 6/2012 Zur Ausgabe

Letter to the Editor

Gluten-Free Diet in Obese Patients with Celiac Disease: An Enemy of the Bariatric Surgeon?

Editorial

A Call for Maintaining Ethical Behavior in Bariatric Surgery

Clinical Research

Obesity and Inflammation: Change in Adiponectin, C-Reactive Protein, Tumour Necrosis Factor-Alpha and Interleukin-6 After Bariatric Surgery

Clinical Research

Screening of Adult ADHD Among Patients Presenting for Bariatric Surgery

Short Communication

Effect of Laparoscopic Adjustable Gastric Banding on Modifiable Cardiovascular Risk Factors in Extremely Obese Adolescents

Clinical Research

Gastroesophageal Reflux after Vertical Banded Gastroplasty is Alleviated by Conversion to Gastric Bypass

Neu im Fachgebiet Chirurgie

Wie erfolgreich ist eine Re-Ablation nach Rezidiv?

23.04.2024 Ablationstherapie Nachrichten

Nach der Katheterablation von Vorhofflimmern kommt es bei etwa einem Drittel der Patienten zu Rezidiven, meist binnen eines Jahres. Wie sich spätere Rückfälle auf die Erfolgschancen einer erneuten Ablation auswirken, haben Schweizer Kardiologen erforscht.

Hinter dieser Appendizitis steckte ein Erreger

23.04.2024 Appendizitis Nachrichten

Schmerzen im Unterbauch, aber sonst nicht viel, was auf eine Appendizitis hindeutete: Ein junger Mann hatte Glück, dass trotzdem eine Laparoskopie mit Appendektomie durchgeführt und der Wurmfortsatz histologisch untersucht wurde.

Mehr Schaden als Nutzen durch präoperatives Aussetzen von GLP-1-Agonisten?

23.04.2024 Operationsvorbereitung Nachrichten

Derzeit wird empfohlen, eine Therapie mit GLP-1-Rezeptoragonisten präoperativ zu unterbrechen. Eine neue Studie nährt jedoch Zweifel an der Notwendigkeit der Maßnahme.

Ureterstriktur: Innovative OP-Technik bewährt sich

19.04.2024 EAU 2024 Kongressbericht

Die Ureterstriktur ist eine relativ seltene Komplikation, trotzdem bedarf sie einer differenzierten Versorgung. In komplexen Fällen wird dies durch die roboterassistierte OP-Technik gewährleistet. Erste Resultate ermutigen.

Update Chirurgie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen

Aktuelle BDC Leitlinien-Webinare

S3-Leitlinie „Diagnostik und Therapie des Karpaltunnelsyndroms“

Karpaltunnelsyndrom BDC Leitlinien Webinare
CME: 2 Punkte

Das Karpaltunnelsyndrom ist die häufigste Kompressionsneuropathie peripherer Nerven. Obwohl die Anamnese mit dem nächtlichen Einschlafen der Hand (Brachialgia parästhetica nocturna) sehr typisch ist, ist eine klinisch-neurologische Untersuchung und Elektroneurografie in manchen Fällen auch eine Neurosonografie erforderlich. Im Anfangsstadium sind konservative Maßnahmen (Handgelenksschiene, Ergotherapie) empfehlenswert. Bei nicht Ansprechen der konservativen Therapie oder Auftreten von neurologischen Ausfällen ist eine Dekompression des N. medianus am Karpaltunnel indiziert.

Prof. Dr. med. Gregor Antoniadis
Berufsverband der Deutschen Chirurgie e.V.

S2e-Leitlinie „Distale Radiusfraktur“

Radiusfraktur BDC Leitlinien Webinare
CME: 2 Punkte

Das Webinar beschäftigt sich mit Fragen und Antworten zu Diagnostik und Klassifikation sowie Möglichkeiten des Ausschlusses von Zusatzverletzungen. Die Referenten erläutern, welche Frakturen konservativ behandelt werden können und wie. Das Webinar beantwortet die Frage nach aktuellen operativen Therapiekonzepten: Welcher Zugang, welches Osteosynthesematerial? Auf was muss bei der Nachbehandlung der distalen Radiusfraktur geachtet werden?

PD Dr. med. Oliver Pieske
Dr. med. Benjamin Meyknecht
Berufsverband der Deutschen Chirurgie e.V.

S1-Leitlinie „Empfehlungen zur Therapie der akuten Appendizitis bei Erwachsenen“

Appendizitis BDC Leitlinien Webinare
CME: 2 Punkte

Inhalte des Webinars zur S1-Leitlinie „Empfehlungen zur Therapie der akuten Appendizitis bei Erwachsenen“ sind die Darstellung des Projektes und des Erstellungswegs zur S1-Leitlinie, die Erläuterung der klinischen Relevanz der Klassifikation EAES 2015, die wissenschaftliche Begründung der wichtigsten Empfehlungen und die Darstellung stadiengerechter Therapieoptionen.

Dr. med. Mihailo Andric
Berufsverband der Deutschen Chirurgie e.V.
Bildnachweise