Pathophysiology of Bariatric Pathophysiology of Bariatric SurgerySurgery

DR SREEJOY PATNAIKBARIATRIC AND METABOLIC SURGEON

LIFE MEMBER OSSI,IFSO,SAGES

SHANTI MEMORIAL HOSPITAL PVT.LTDFinal Phase of NABH Accredition.

Obesity EpidemicObesity Epidemic

• World epidemic encompasses 1.7 billion people

• Highest in the U.S.

• Approximately 2/3 of Americans are overweight, and almost half are obese

• BMI subgroups of >35 and >40 are experiencing most rapid growth

Buchwald et al. Jama 2004Buchwald et al. Jama 2004

Obesity EpidemicObesity Epidemic

• Rise in the prevalence of obesity is associated with rises in prevalence of obesity related comorbidities

• Comorbidities responsible for 2.5 million deaths per year worldwide

• Loss of life expectancy is profound• 25 year-old morbidly obese male has 22%

reduction in lifespan, representing a loss of 12 years of life

Buchwald et al. Jama 2004Buchwald et al. Jama 2004

Obesity EpidemicObesity Epidemic

• Diet therapy, with and without support organizations, is ineffective long term

• Currently, there are no effective pharmaceutical agents to treat obesity, especially morbid obesity

North American Association for the North American Association for the Study of Obesity. NIH 2000Study of Obesity. NIH 2000

Definition of Obesity Definition of Obesity according to BMIaccording to BMI

UnderweightUnderweight <18.5<18.5

NormalNormal 18.5 – 24.918.5 – 24.9

OverweightOverweight 25-29.925-29.9

ObesityObesity >30>30

moderate moderate 30.0 – 34.930.0 – 34.9

severesevere 35.0 – 39.935.0 – 39.9

morbidmorbid >40>40

BMI = W(kg)/H (m²)BMI = W(kg)/H (m²)

BMIBMI

• Calculated as follows: Weight(kg)/Height(m2)

• Lowest mortality = BMI < 25kg/m2

• Highest mortality = BMI > 40kg/m2

• BMI > 40 = approximately 100lbs. over ideal body weight

Why Operate?Why Operate?

Pulmonary diseaseabnormal functionobstructive sleep apneahypoventilation syndrome

Nonalcoholic fatty liver diseasesteatosissteatohepatitiscirrhosis

Coronary heart disease Diabetes Dyslipidemia Hypertension

Gynecologic abnormalitiesabnormal mensesinfertilitypolycystic ovarian syndrome

Osteoarthritis

Skin

Gall bladder disease

Cancerbreast, uterus, cervixcolon, esophagus, pancreaskidney, prostate

Phlebitisvenous stasis

Gout

Medical Complications of ObesityIdiopathic intracranial hypertension

Stroke

Cataracts

Severe pancreatitis

Medical Co-morbidities

• 1.Metabolic 2.Mechanical 3.Degenerative 4.Neoplastic 5.Psychological

Medical Co-morbiditiesMetabolic

Diabetes mellitus, type II Hypertriglyceridemia Hypercholesterolemia Hypertension Gallstones Fatty liver disease (NASH) Pancreatitis Central sleep apnea Hypercoagulable Infertility

Metabolic Syndrome

Abdominal obesityHyperinsulinemiaHigh fasting plasma glucoseImpaired glucose toleranceHypertriglyceridemiaLow HDL-cholesterolHypertension

Medical Co-morbiditiesMechanical/Anatomic

Obstructive sleep apnea GERD GERD - associated asthma Urinary stress incontinence Pseudotumor cerebri Venous stasis DVT / PE Fungal skin infections Decubitus ulcers Accidental injuries

Medical Co-morbiditiesDegenerative

Cardiovascular disease Complications of diabetes CHF Vertebral disc disease NASH related cirrhosis

Medical Co-morbiditiesNeoplastic

Breast Cancer Ovarian Cancer Endometrial Cancer Prostate Cancer Colorectal Cancer Renal Cell Carcinoma NHL Esophageal Cancer Gastric Cancer Pancreatic Cancer

Medical Co-morbiditiesPsychological

Anxiety disorders Depression Binge eating disorders Reactive bulimia Trauma

Indications for SurgeryIndications for Surgery

• BMI > 40 kg/m2BMI > 40 kg/m2• BMI > 35 kg/m2 with 2 co-morbiditiesBMI > 35 kg/m2 with 2 co-morbidities

• Comorbidities:Comorbidities:– HypertensionHypertension– DiabetesDiabetes– HyperlipidemiaHyperlipidemia– Sleep apneaSleep apnea– Severe arthrosisSevere arthrosis

NIH Consensus NIH Consensus Conference Conference Ann Intern Med 1991Ann Intern Med 1991

Indications for SurgeryIndications for Surgery

• Age > 18 or < 60Age > 18 or < 60• Failure of diet > 6 monthsFailure of diet > 6 months• Obesity history > 5 Obesity history > 5 yearsyears • Low risk for surgeryLow risk for surgery• No endocrinological diseaseNo endocrinological disease• Psychologically soundPsychologically sound

NIH Consensus Conference NIH Consensus Conference Ann Intern Med 1991Ann Intern Med 1991

Goals of SurgeryGoals of Surgery

• Effective: Loss > 50% of Excess Effective: Loss > 50% of Excess WeightWeight

• Low operative morbidityLow operative morbidity

• Well toleratedWell tolerated

• No long term complicationsNo long term complications

Surgical ProceduresSurgical Procedures

• Restrictive proceduresRestrictive procedures– Gastric BandingGastric Banding– Sleeve GastrectomySleeve Gastrectomy– -Gastric Plication-Gastric Plication

• Malabsorptive proceduresMalabsorptive procedures– Biliopancreatic DiversionBiliopancreatic Diversion

• ScopinaroScopinaro• Duodenal-Switch BPDDuodenal-Switch BPD

• Hybrid proceduresHybrid procedures– Roux-en-Y Gastric Bypass / BandedRoux-en-Y Gastric Bypass / Banded– -Mini Gastric Bypass-Mini Gastric Bypass

Bariatric Procedures Performed Today

BBilio-pancrilio-pancreeatiatic diversionc diversion

ScopinaroScopinaro SGWithSGWith duodenalduodenal switchswitch

How does a sleeve work?

One of the mechanisms involved in weight loss observed after the LSG is the dramatic reduction of the capacity of the stomach.

Ghrelin A peptide hormone mainly produced in the fundus of the stomach, is supposed to be involved in the mechanisms regulating hunger .

Secreted by the endocrine cells of the stomach (X/A-like cells), which reside in the oxyntic glands of the gastric fundus .

It regulates the secretion of growth hormone release and is a potent orexigenic (appetite-stimulating) peptide & is mediated by the activation of ghrelin receptors in the hypothalamus / pituitary area .

Plasma concentration rises just before the onset of meal and declines after intake of meals .

Plays a key role in the complex energy balance and certain neurophysiologic mechanisms are responsible for the changes in appetite observed after bariatric surgery

Restriction

Malabsorption

Gastric Bypass

Loss of appetite ?Small pouch (approx 30 cc)

Small anastomosis (approx. 1.5 cm)

How does it work ?

Alimentary LimbBetween 100 to 200cm

Biliopancreatic LimbBetween 50 to 75 cm

Ghrelin

Pathophysiology of Bariatric Surgery of Bariatric Surgery

• Role of GI Hormones in remission of Metabolic syndrome.

• Recent theory- Entero-insular axis has got a role in maintaining glucose homeostasis.

• Bariatric surgery results in weight loss due to surgical manipulation or bypassing of the gut & by caloric restriction

- leading to remission of metabolic syndrome.

GI HORMONES AS INCRETINS & ANTI INCRETINS

WHAT ARE incretins ?

• Incretins are a group of gastrointestinal hormones that increase the amount of insulin release from the beta cells after eating.

• They also slow the rate of absorption of nutrients into the blood stream by reducing gastric emptying and reduces food intake.

• Inhibits Glucagon release from the alpha cells of the Islets of Langerhans.

• 1. GLP-1- Glucagon-like peptide-1 • 2 . GIP- Gastric inhibitory peptide or Glucose-

dependent insulinotropic polypeptide

Mechanism of Incretin action action

WHAT ARE ANTI INCRETINS?

• Anti incretins are a group of GI factors secreted from the duodenum & proximal jejunum, which counteract the actions of INCRETINS.

Anti incretin action

ANTI INCRETINS AND GLUCOSE HOMEOSTASIS

GUT BRAIN AXISThe gut–brain axis is a major component of appetite regulation.

The gut hormones have either • anorexigenic ( appetite depressant ) or • orexigenic ( appetite stimulant ) action on food intake .

•These gut hormone secretions are altered following bariatric surgery

• GHRELIN - (orexrgenic / satiety or appetite stimulant hormone)

Peptide YY – an anorexegenic (or appetite depressant) hormone co-secreted with GLP-1 from the intestinal L

cells in response to food intake.

• PYY3-36 - ( anorxegenic hormone ) -levels are increased following LRYGB, decreases food

intake & ameliorates insulin resistance and improves glycemia.

PROPOSED THEORIES FOR IMPROVED GLYCAEMIA

(A) RAPID HINDGUT DELIVERY HYPOTHESIS

•Expedited or rapid delivery of ingested nutrients to lower bowel due to intestinal bypass leads to stimulation of L cells, ( distal ileum & colon ) which in turn results in increased secretion of incretin hormones & improved glucose homoeostasis. (LRYGB & BPD/DS.)

•Proximal nutrient- related signals that are transmitted from the duodenum to the distal bowel by neural pathways leads to

increased Incretin secretion.

PROPOSED T(B) FOREGUT HYPOTHESIS HEORIES FOR IMPROVED

GLYCAEMIA

•The proximal small intestine (foregut / BPD limb ) is excluded resulting in reduction in secretion of Anti – incretin factors ( diabetogenic hormones) in response to absence of nutrients in the fore gut.

•This leads to improved glycaemia. &•Decreased Intestinal Glucagon synthesis .

ANTI-INCRETIN / INCRETIN BALANCE

• After Bariatric Surgery - a physiological balance is maintained between Anti –Incretins & Incretins,

• Leads to proper beta cell function & to maintain Blood Glucose excursions within normal range.

• Release of excess Anti- Incretins are prevented leading to improved glucose homeostasis.

Diabetes, Obesity & Bariatric surgery

• DM linked with obesity has – -- insulin resistance, inflammation & lipo-toxicity of beta cells, > progressive beta cell failure & hyper-glycaemia.

•After Bariatric Surgery - - Glucose homeostasis improves.

- Insulin sensitivity increases. - Adiponectin levels improves - Markers of insulin signals in key target tissues are enhanced.

Hypothesis as to the mechanism responsible for the control of diabetes after gastric bypass.

MY ExperienceS iN Bariatric Surgery

Bariatric Procedures (n=40) 2010

• Lap adjustable gastric band 0

• Lap sleeve gastrectomy 35

• Lap gastric bypass 2

• Lap duodenal switch 0

• Lap gastric plication 0

• Ileal Transposition 0

• Revisional Bariatric procedure 1

• MGB 2

OUR SUCCESSFUL PATIENTS

KENDRAPARA

THE MOST ELIGIBLE BACHELOR

CUTTACK -- FIRST CASE

CUTTACK

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HAPPY AFTER MARRIAGE

BHAWANIPATNA

CUTTACK

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Conclusion

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