Obesity Anesthesia Considerations

  • Obesity Statistics:

    • 2nd leading cause of preventable death in the U.S.

    • Increased risk of medical and surgical complications and mortality:

      • Diabetes Mellitus (DM)

      • Hypertension (HTN)

      • Hyperlipidemia

      • Obstructive Sleep Apnea (OSA)

      • Non-Alcoholic Fatty Liver Disease (NAFLD)

      • Cholelithiasis (gallstones)

  • Definition of Obesity:

    • Body Mass Index (BMI):

      • Obese: BMI > 30

      • Morbid/Extreme Obesity: BMI > 40

    • Obesity Class

      • Class I: BMI 30-34.9

      • Class II: BMI 35-39.9

      • Class III: BMI >40

  • Types of Obesity:

    • Central/Abdominal Obesity: Increases comorbidities in obese patients.

      • Waist circumference:

        • > 40 in. in Men

        • > 35 in. in Women

      • Increased risk for:

        • Ischemic Heart Disease

        • Diabetes Mellitus

        • Hypertension

        • Dyslipidemia

        • Death

    • Gluteal/Femoral Obesity: Increases risk of varicose veins and joint issues

  • Genetic Influence on Obesity:

    • Approximately 40% of body mass results from genetic influence

    • Environmental factors account for around 60%

    • Weight loss decreases comorbidity risk

Anesthesia Considerations for Obesity

  • Challenges in Administration:

    • Difficulties in identifying landmarks for regional anesthesia

    • Use of Point of Care Ultrasound (POCUS) may be indicated

    • Consideration for longer epidural needles (7 inches)

  • Local Anesthesia Administration:

    • Caution to avoid cephalic spread during neuraxial anesthesia

    • Keep patient in an upright position for a short time post-administration to reduce risks

  • Post-operative Opioid Use:

    • Increased risk for respiratory depression

Non-Alcoholic Fatty Liver Disease (NAFLD)

  • Definition:

    • Disease similar to alcohol-induced hepatic dysfunction characterized by:

    • Hepatomegaly related to fatty infiltrates (Steatohepatitis)

  • Symptoms: Typically asymptomatic, may be discovered through abnormal liver enzyme levels or imaging

  • Diagnosis: Liver Biopsy

  • Risk Factors:

    • Central obesity

    • Insulin resistance

  • Treatment:

    • Surveillance

    • Encouragement of weight loss and exercise

  • Complications: Increased risk for cirrhosis, portal hypertension, and liver carcinoma

Cholelithiasis (Gallstones)

  • Pathophysiology:

    • Gallstones form due to increased cholesterol in bile and altered bile salt ratios

    • Potential for pain and blockage of bile duct

  • Symptoms:

    • Epigastric pain radiating to the shoulder blades

    • Colicky pain associated with eating

    • Jaundice

  • Diagnosis: AST/ALT, Bile Salts, Amylase, Lipase, Abdominal Ultrasound

  • Risk Factors:

    • 30% increased prevalence of gallstones in obese patients

    • Higher BMI correlates with higher risk

  • Treatment Options:

    • Surgical intervention preferred; laparoscopic methods over open surgery

    • Intraop fluid replacement to aide with PONV

Pancreas Pathophysiology Review

  • Overview of the Pancreas:

    • A retroperitoneal organ with both endocrine and exocrine functions

    • Islets of Langerhans are responsible for endocrine functions

      • Composed of various cell types:

        • α Cells: Secrete glucagon

        • β Cells: Secrete insulin into liver circulation

        • Insulin reduced by 50% due to first-pass effect

      • Glucagon and insulin regulate carbohydrate, protein, and fat metabolism

  • Insulin Functions:

    • Released from β cells when Blood Glucose (BG) > 100 mg/dL

    • Causes storage of carbohydrates, proteins, and fats when supplies are low

    • Removes glucose from circulation; stores it in liver as glycogen

    • Peaks at levels within 30 - 60 minutes post-eating

  • Glucagon Functions:

    • secreted by α cells when BG < 90 mg/dL

    • Acts as a biological antagonist to insulin

Pancreas Pathophysiology in Fasting vs Eating

  • Metabolism During Fasting:

    • Decreased Insulin = suppresses glucose released back into circulation

    • Decreased insulin = Triglycerides are broken down into free fatty acids, which then enter circulation and oxidize in the liver to form ketones

      • Pronounced concentration occurs with long periods of fasting (aka, DKA with fruity breath)

  • Metabolism During Eating:

    • Increased Insulin = glucose removed from plasma and stored in liver as glycogen

    • Increased insulin = prevents triglycerides breakdown

Diabetes Mellitus Overview

  • Definition:

    • A metabolic disorder caused by Insulin deficiency leading to impaired metabolism of carbohydrates, proteins, and fats

    • Glucose is available due to lack of insulin but cannot be stored in cells (stays in serum)

  • Symptoms:

    • Polydipsia (excessive thirst)

    • Polyphagia (excessive hunger)

    • Polyuria (excessive urination)

  • Diagnosis:

    • A1C > or equal to 6.5% OR

    • fasting plasma glucose > or equal to 126 mg/dL OR

    • 2-hr plasma glucose > or equal to 200 mg/dL during oral glucose tolerance test with 75 g anhydrous glucose dissolves in water OR

    • Random plasma glucose > or equal to 200 mg/dL in patients with s/s of hyperglycemia

  • Risk Factors:

    • Obesity

    • Sedentary lifestyle

    • Elderly age

  • Types of Diabetes Mellitus:

    • Type 1 Diabetes Mellitus (DM1)

    • Type 2 Diabetes Mellitus (DM2)

  • Complications:

    • Hypertension

    • Retinopathy

    • Neuropathy

    • Cardiovascular Disease (CVD)

    • Coronary Artery Disease (CAD)

    • Stroke

    • Myocardial Infarction (MI)

Diabetes Mellitus Type 1 (DM1)

  • Pathophysiology:

    • Autoimmune destruction of β cells, resulting in absolute insulin deficiency

    • Causes include infections or immune assaults

  • Consequences of Insulin Deficiency:

    • As insulin secretion declines, excess glucose is released from the liver

    • Once BG levels exceed 200 mg/dL, kidneys cannot reabsorb glucose, resulting in glucosuria

    • Elevated glucose levels lead to polyuria (excessive urination)

    • Leads to intracellular dehydration, causing polydipsia (excessive thirst)

    • Triglyceride breakdown increases glycerol in circulation, raising lipid levels and atherosclerosis risk

  • Prevalence:

    • DM1 accounts for only 5% of diabetes patients

    • Typically develops by age 30

  • Tx: daily exogenous insulin administration for the lifetime

Diabetes Mellitus Type 2 (DM2)

  • Pathophysiology:

    • Characterized by impaired insulin secretion due to insulin resistance

    • As insulin secretion declines, there is excess glucose release from the liver

  • Consequences of Insulin Resistance:

    • Glucose level exceeds 200 mg/dL, leading to glucosuria as kidney can no longer capture and reabsorb glucose

    • Polyuria acts as a diuretic

    • intracellular dehydration causes polydipsia

    • Increased triglyceride breakdown results in higher glycerol levels and increased risk for atherosclerosis

  • Prevalence: Accounts for 95% of diabetes patients

  • Risk Factors:

    • Obesity

    • Age 50-60 years

    • Family history

    • NAFLD

  • Treatment Options:

    • Oral glucose-lowering agents

    • Exercise

    • Weight loss

    • Exogenous insulin

Anesthesia Considerations

  • Preop EKG

  • Preop aspiration prophylaxis with gastroprokinetic agents, e.g., Reglan

  • Core temperature monitoring is essential due to risks of hypothermia from autonomic neuropathy

  • Thickened tissues may cause Stiff Joint Syndrome:

    • Limited head/neck flexion, extension, and lateral extension

    • The prayer sign indicates difficulty with airway

  • Hold oral hypoglycemic medications on the day of surgery; sliding scale insulin (SSI) or insulin pumps can continue until the surgery day

  • Baseline Labs:

    • Urinalysis (UA)

    • Serum Creatinine

    • Blood Urea Nitrogen (BUN)

    • Fasting Blood Glucose (FBG) on the morning of surgery

    • Hemoglobin A1C

    • Comprehensive Metabolic Panel (CMP)

  • Schedule procedures earlier in the day to limit disruption of treatment regimen and nutrition needs

  • Address decreased tissue perfusion by focusing on patient positioning and padding

  • BG monitoring, Insulin, and IV dextrose titration/balance during procedures exceeding 1 hour

    • Hourly POC is ok for stable patients

    • Serum BG hourly for brittle, unstable patients

Diabetes Mellitus Complications

  • Hypoglycemia:

    • Common with exogenous insulin or oral hypoglycemic agents, especially in NPO status; can lead to brain damage if untreated

    • Symptoms include:

      • Tachycardia

      • Diaphoresis

      • Anxiety

      • Tremors

      • Pupil dilation

      • Note: General anesthesia can mask symptoms

    • Diagnosis: BG < 50

    • Treatment:

      • Administer IV dextrose to achieve BG > 100 if IV access is available

      • If no access, administer glucagon

  • Diabetic Ketoacidosis (DKA):

    • Characterized by hyperglycemia, ketonemia, and acidemia; often triggered by noncompliance with insulin therapy, critical illness, or infection

    • Most common in DM1

    • Symptoms include:

      • Rapid, deep breathing (Kussmaul respirations)

      • Fruity smell of breath

      • Coma

    • Dx: BG >250, lactic acidosis, ketone presence

    • Tx: insulin, tx underlying infection or illness