ANAESTHETIC CONSIDERATIONS IN DIABETES MELITUS2.pptx

Management and anaesthetic consideration in diabetic patients

1. ANAESTHETIC CONSIDERATIONS IN DIABETES MELLITUS PRESENTOR – DR RAJESH KANNAN MODERATOR –DR SHIPRA VERMA UPUMS, SAIFAI

2. DIABETES MELLITUS INTRODUCTION CLASSIFICATION PATHOGENESIS TREATMENT COMPLICATIONS ANAESTHETIC MANAGEMENT PREOPERATIVE INTRAOPERATIVE POSTOPERATIV E

3. DIABETES MELLITUS Diabetes is a disorder of impaired glucose metabolism that results from inadequate supply of insulin , inadequate response to insulin or combination of both, the hallmark of the disease is increased circulating levels of serum glucose when left untreated lead to diffuse microvascular and macrovascular complications leading to end organ dysfunction.

4. PATHOPHYSIOLOGY The body obtains glucose from three main places Intestinal absorption of food Breakdown of Glycogen the storage form of glucose found in liver Gluconeogenesis is the generation of glucose from non-carbohydrate substrates in the blood

5. Insulin is the principal hormone that regulates the uptake of glucose from blood into cells of the body, especially in liver, adipose tissue, muscle except in smooth muscle in which insulin acts via Insulin like growth factors (IGF -1),via tyrosine kinase pathway Therefore deficiency of insulin or insulin insensitivity of its receptors plays a central role in all forms of Diabetes mellitus PATHOPHYSIOLOG Y

6. PATHOPHYSIOLOGY If the amount of insulin available is insufficient and there is resistance to action of insulin Glucose will not be absorbed by body cells Net effect is high levels of blood glucose, poor protein synthesis, break down of fat storage resulting in formation of ketone bodies resulting in acidosis

7. PATHOPHYSIOLOGY When glucose concentration in blood remains high over time, kidneys will reach threshold above for glucose reabsorption resulting in glycosuria Resulting in osmotic diuresis , and increase in osmotic pressure, resulting in fluid loss Lost blood volume will be replaced osmotically, from water held in other compartments of the body resulting in dehydration and polydipsia

8. CLASSIFICATION PRIMARY Type 1 Diabetes mellitus Type 2 Diabetes mellitus Gestational Diabetes mellitus SECONDARY Drug induced (steroids, phenytoin, betta blockers , thiazides, doxorubicin) Infections Endocrinopathies ( cushings syndrome , pheochromocytoma, acromegaly)

9. TYPE 1 DIABETES MELLITUS Causes Absolute insulin deficiency caused by Autoimmune T cell mediated destruction of pancreatic betta cells by genetic (MHC class 2),viruses (cox, rubella), environmental factors characterized by insulin deficiency has an incidence of 5%-10% in childhood. Clinical features Polyuria, Polydipsia, Loss of weight, Fatigue, Weight loss Patients are more prone for ketosis

10. TYPE 2 DIABETES MELLITUS Characterized by relative deficiency of insulin / peripheral resistance to insulin , incidence of 90% in all cases of Diabetes mellitus and in obese adults characterized by beta cell insufficiency, patients produce adequate amount of insulin to prevent ketosis but are at risk of Hyperglycemic Hyperosmolar coma Clinical features Polyuria, polydipsia, polyphagia, weight gain Risk factors Genetic, Age , obesity , sedentary lifestyle

11. PATHOGENISIS OF DIABETES MELLITUS

12. DIAGNOSTIC CRITERIA FOR DIABETES MELLITUS Symptoms of diabetes (polyuria , polydipsia , unexplained weight loss ) plus a random blood glucose concentration or Fasting (no caloric intake for 8 hours) plasma glucose level 126 mg/dl or Two hour plasma glucose level 200 mg/dl during an oral glucose tolerance test  

13. CRITERIA FOR DIAGNOSIS OF PRE DIABETES

14. GESTATIONAL DIABETES MELITUS Pregnancy is diabetogenic state characterized by progressive peripheral resistance to insulin at receptor and post receptor levels in second, third trimesters due to increase in hormones such as placental lactogen, growth hormone, cortisol, progesterone. Gestational diabetes mellitus develops when a patient cannot mount a compensatory insulin response during pregnancy. Gestational diabetes mellitus is a preclinical state of glucose intolerance that is not detectable before pregnancy. After delivery most patients return to normal glucose tolerance but remain at increased risk for Diabetes mellitus.

15. TWO STEP STRATEGY STEP 1 -Perform a non fasting 50 gram oral glucose load test with plasma glucose measurement at end of 1 hour at 24 to 28 weeks gestation in women not previously diagnosed with overt Diabetes mellitus if plasma Glucose 1 Hour after glucose load 130 mg /dl STEP 2 -100 gram oral glucose tolerance test done with 8 Hour fasting, four blood samples at fasting, 1 hour, 2 hour, 3 hour intervals; diagnosed with Gestational DM if two of four plasma glucose levels exceed the criteria   SAMPLE BLOOD GLUCOSE LEVEL Fasting 105 mg/dl 1 hour 180mg/dl 2 hours 155 mg/dl 3 hours 140 mg/dl SAMPLE BLOOD GLUCOSE LEVEL Fasting 1 hour 2 hours 3 hours

16. GLYCEMIC TARGETS IN PREGNANCY ADA GUIDELINES TIME OF BLOOD SUGAR TARGET FOR WOMEN WITHOUT PREEXISTING TYPE 1 & 2 DIABETES MELLITUS TARGETS FOR WOMEN WITH PREEXISTING TYPE 1 & 2 DIABETES MELLITUS FASTING 95 mg/dl 60-90 mg/dl 1HOUR POST PRANDIAL 140 mg/dl 100-129 mg/dl 2HOUR POST PRANDIAL 120 mg/dl 100 mg/dl TIME OF BLOOD SUGAR TARGET FOR WOMEN WITHOUT PREEXISTING TYPE 1 & 2 DIABETES MELLITUS TARGETS FOR WOMEN WITH PREEXISTING TYPE 1 & 2 DIABETES MELLITUS FASTING 60-90 mg/dl 1HOUR POST PRANDIAL 100-129 mg/dl 2HOUR POST PRANDIAL

17. METABOLIC SYNDROME Fasting plasma glucose level mg/dl Abdominal obesity (waist girth >40 inches in men , >35 inches in women ) Serum triglycerides 150mg/dl Blood pressure 130/85 mm hg More than any of the three features is regarded as metabolic syndrome  

18. TREATMENT OF DIABETES MELLITUS

19. TYPE OF DRUG MECHANISM EXAMPLES ADVANTAGES DISADVANTAGES CONTRAINDICATION Biguanides Decrease Hepatic Glucose production & increase peripheral glucose uptake Metformin Phenformin Weight loss Lactic acidosis , Diarrhea , nausea Serum creatinine > 1.5mg/dl CHF, metabolic acidosis Alpha Glucosidase inhibitors Reduce glucose absorption Acarbose ,Miglitol Reduce postprandial glycemia Flatulence Deranged LFT Renal/Liver disease Dipeptidyl Peptidase IV inhibitors Prolong endogenous GLP 1 action increase incretin Sitagliptin saxagliptin Weight loss pancreatitis Reduce dose with renal disease Insulin Secretagogues- sulfonylureas Increase insulin secretion Glipizide Glibenclamide Short onset of action lowers postprandial glucose Hypoglycemia weight gain Renal/ Liver disease Insulin Secretagogues- Non sulfonylureas Increase insulin secretion Repaglinide Nateglinide Short onset of action lowers postprandial glucose Hypoglycemia Renal/Liver disease Thiazolidinediones Increase glucose sensitivity, PPAR gamma agonist Pioglitazone Lowers insulin requirements Peripheral edema , CHF, weight gain Congestive heart failure Liver disease

20. ACUTE EFFECTS OF HYPERGLYCEMIA Dehydration and electrolyte disturbance (due to osmotic diuresis) Acidemia (accumulation of lactic + ketoacids) Fatigue ,weight loss and muscle wasting (lipolysis and proteolysis in absolute insulin deficiency) Poor wound healing and impaired wound strength Diabetic ketoacidosis (Type I Diabetics due to absolute insulin deficiency ) Hyperosmolar Non- ketotic coma ( Type II Diabetics)

21. DIABETIC KETOACIDOSIS Diabetic ketoacidosis (DKA) is usually seen in insulin-dependent diabetic patients. The definition of DKA proposed by the American Diabetes Association Serum glucose level mg/dl Ph 7.3 Hco3 18 mEq /L Serum osmolarity <320 mOsm /L Serum and urine ketone levels- Moderate to high  

22. MANAGEMENT Intravenous Fluids Start with isotonic saline at 1 L/ hr (15–20 mL/kg/ hr ) When blood glucose falls to 250 mg/dL, change to 5% dextrose with Insulin infusion Insulin Regular insulin: 0.15 units/kg as an IV bolus, then infuse at 0.1 units/kg/ hr Adjust infusion so that blood glucose decreases by 50–75 mg/dL per hour When blood glucose reaches 250 mg/dL, decrease infusion rate to 0.05 units/kg/ hr , and maintain blood glucose at 150–200 mg/dL Begin SC insulin when DKA resolves when pH> 7.3,Hco3>18mEq/L .

23. ELECTROLYTE MANAGEMENT Serum potassium ADVISE < 3.3 mEq /l Hold the insulin infusion and give 20-30 mEq K+ /hour until the [K+] is ≥ 3.3 mEq /L 3.3–4.9 mEq /l Give 20–30 mEq K+/hour in IV fluid to keep serum [K+] at 4–5 mEq /L. ≥ 5 mEq /l Do not give K+, check serum [K+] every 2 hours.

24. NON KETOTIC HYPEROSMOLAR HYPERGLYCEMIC STATE (NKHSS) Diagnostic features Plasma glucose >600mg/dl Ph>7.3 Hco3>15mEq/L Serum osmolarity>350mOsm/L Incidence Patients with Type 2 diabetes mellitus commonly with age more than 60years Clinical features Polyuria, Polydipsia, Hypotension, Hypovolemia

25. MANAGEMENT Initial treatment involves administration isotonic saline 1-2 litres /15-20 ml/kg/ hr /iv Insulin infusion - 0.14 U/kg/hr as continuous infusion Serum glucose – 300mg/dl reduce insulin infusion rate to 0.02-0.05U/kg/ hr /iv Blood glucose (BG) Monitoring: 1. Goal of decrease in blood glucose : 50-75 mg/dl/hr (hourly monitor) 2. Once stable 2 hourly BG monitoring 3. Add dextrose 5% when BG less than 250 mg/dl. For DKA: Goal BG: 150-200 mg/dl For HHS: Goal BG: 250-300 mg/dl

26. CHRONIC EFFECTS OF HYPERGLYCEMIA MICROVASCULAR COMPLICATIONS Diabetic nephropathy Neuropathy Retinopathy MACROVASCULAR COMPLICATIONS Coronary artery disease Peripheral vascular disease Cerebrovascular stroke

27. CARDIOVASCULAR SYSTEM: Diabetic patients are at increased risk for hypertension , coronary artery disease , congestive Heart failure ,cerebrovascular , peripheral vascular disease due to atherosclerosis and endothelial damage Diabetic patients may have clinically silent Myocardial ischemia and infraction

28. DIABETIC NEPHROPATHY: MECHANISM 1.Glomerular hyperfiltration 2.Increase in glomerular hydrostatic pressure causes glomerular damage and microalbuminuria 3.Impaired endothelium dependent vasodilatation earliest sign is microalbuminuria (albumin >300mg/dl/day)

29. PERIPHERAL NEUROPATHY: Include local ischemia , tissue accumulation of sorbitol altered function of neuronal Na+/k+ ATPase A Distal symmetric diffuse sensory motor polyneuropathy is the most common form Sensory deficits usually appear in Glove and stockings pattern Loss of large sensory and motor fibers produces loss of light touch and proprioception as well as muscle weakness Loss of small fibers of Lateral spinothalamic tract results in loss of response to pain and temperature

30. AUTONOMIC NEUROPATHY: Orthostatic hypotension Resting tachycardia Gastroparesis (vomiting , diarrhea ) Impotence Asymptomatic hypoglycemia

31. TESTS FOR DIABETIC NEUROPATHY Heart rate variability (HRV) in response to: Deep breathing Standing Valsalva maneuver BP response to : Standing or passive tilting Sustained hand grip Valsalva maneuver

32. HEART RATE VARIABILITY (HRV) IN RESPONSE TO DEEP BREATHING: Respiratory sinus arrhythmia is a normal phenomenon due to vagal input to sinus node during expiration causing cardio deceleration The patient lies quietly and breathes deeply at a rate of 6/min ECG monitor records the difference between the maximum and minimum heart rates Normal variability: >15 beats/min Abnormal variability: <10 beats/min

33. EFFECT OF STANDING ON HEART RATE : This test evaluates the cardiovascular response elicited by a change from a horizontal to a vertical position Standing causes r apid increase in heart rate that is maximal at approximately the 15th beat R elative bradycardia that is maximal at approximately the 30th beat after standing The patient is connected to an ECG monitor while lying down and then stands to a full upright position

34. EFFECT OF STANDING ON HEART RATE: ECG tracings measured at 30:15 ratio calculated as the ratio of the longest R-R interval the shortest R-R interval found at and beat   RATIO OF RR INTERVAL INTERPRETATION > 1.04 NORMAL 1.01-1.03 BORDERLINE 1.01 ABNORMAL

35. VALSALVA MANEUVER: supine patient, connected to an ECG monitor and forcibly exhales into the mouthpiece of a manometer, exerting a pressure of 30 mm Hg for 15 seconds with an open glottis. The Valsalva Ratio is determined from the ECG tracings by calculating the ratio of the longest R-R interval after the maneuver (reflecting the bradycardic response to blood pressure overshoot) to the shortest R-R interval during or shortly after the maneuver (reflecting tachycardia as a result of strain). Ratio < 1.2 is abnormal Ratio>1.2 Normal

36. ORTHOSTATIC HYPOTENSION: Orthostatic hypotension is defined as a decrease in SBP of 20 mm Hg or a decrease in DBP of 10 mm Hg within 3 minutes of standing when compared with blood pressure from the sitting or supine position Alternatively, the diagnosis can be made by head-up tilt-table testing at an angle of at least 60 degrees. BP is rapidly corrected by baroreflex-mediated peripheral vasoconstriction and tachycardia. • A fall of SBP 30 mm Hg ,DBP 10 mm Hg is abnormal • A fall of SBP 10 to 29 mm Hg , DBP 10 mm Hg is borderline  

37. HYPOGLYCEMIA Level 1 Hypoglycemia -<70 mg/dl – 54 mg/dl Symptoms – sweating , palpitations ,tremors Level 2 Hypoglycemia- <54 mg/dl Neuroglycopenic symptoms occur Drowsy , speech difficulty , seizures Level 3 Hypoglycemia – Altered mental functioning Treatment 25g IV Dextrose stat , 50ml Dextrose in 50% Normal saline iv 1mg IM Glucagon if patient is not alert

38. ANAESTHETIC MANAGEMENT PREOP MANAGEMENT INTROP MANAGEMENT POSTOP MANAGEMENT PERIOPERATIVE HYPERGLYCEMIA POSTOPERATIVE HYPOGLYCEMIA

39. EXAMINATION IN DIABETIC PATIENTS Palm Print Test: Palm print test: Stiffness of the 4th and 5th interphalangeal joints causes alteration in palm print The palm and fingers of the dominant hand of the patient is painted with ink Then the hand is firmly pressed on a white sheet of paper on a hard surface Grade 0—All phalangeal areas visible Grade 1—Deficiency in the interphalangeal areas of 4th and 5th digit Grade 2—Deficiency in the interphalangeal areas of 2nd to 5th digit Grade 3—Only the tips of digits seen

40. PRAYER SIGN Prayer sign: Positive prayer sign inability to approximate their palms and fingers while pressing their hands together with fingers extended Prayer sign is most sensitive indicator for predicting for difficult intubation

41. PREOP INVESTIGATIONS Hemoglobin(Hb)-To rule out anemia due to renal dysfunction TLC-To rule out infective pathology Urine routine – for albumin Serum creatinine –To detect renal dysfunction Fasting and postprandial blood sugar – to assess quality of sugar control Glycosylated HB – HBA1C <7% implies good blood sugar control over preceding 8-12 weeks Serum electrolytes – To detect abnormalities in patients with history of vomiting , diarrhea, poor oral intake ,intestinal obstruction ,also in patients on insulin, diuretics and renal dysfunction ECG- To detect asymptomatic myocardial ischemia X ray chest – Tuberculosis is most common in diabetics in india

42. ADVISE ON ORAL HYPOGLYCEMIC AGENTS BEFORE SURGERY

43. ADVISE ON INSULIN BEFORE SURGERY ADVISE ON INSULIN ON DAY OF SURGERY

44. PAC ADVISE CONSIDERATIONS Consent NPO orders (patient should take Half of their short acting insulin dose with 8 Hours for solid and 2 hours for clear liquid) Anxiolytic (tab Alprox 0.5mg HS) Aspiration prophylaxis H2 blockers ( Ranitidine 150mg od), Antiemetics (metoclopramide 15mg Bd) Stop OHA and Insulin according to standard protocol. Morning sample of Blood sugar and s. electrolytes to be sent Planned to take 1 st case in morning to avoid prolong period of NPO.

45. SURGICAL STRESS ON DIABETES MELLITUS

46. METABOLIC CONSEQUENCES OF SURGICAL STRESS The surgical stress stimulus alters finely regulated balance between hepatic glucose production and glucose utilization in peripheral tissues. Surgical stress causes increase in Cortisol which increases hepatic glucose production , stimulates protein catabolism and promotes gluconeogenesis , resulting in elevated blood glucose levels. Catecholamines increases glucagon secretion and inhibits insulin release by pancreatic betta cells Increase in stress hormones leads to enhanced lipolysis and high free fatty acid concentrations which inhibits insulin mediated glucose uptake in liver, increased in Gluconeogenesis, Glycogenolysis and Insulin resistance in skeletal muscles, resulting in Hyperglycemia.

47. IV DRUG CONSIDERATIONS IN DIABETIC PATIENTS FENTANYL Produce hemodynamic, hormonal and metabolic stability e ffectively blocks sympathetic nervous system and the HPA axis resulting in reduced stress response resulting in decreased cortisol reduction ETOMIDATE Blocks adrenal steroidogenesis and hence cortisol synthesis by its action on 11 β-hydroxylase and cholesterol cleavage enzymes And consequently decreases the hyperglycemic response to surgery

48. PROPOFOL: Diabetic patients have a reduced ability to clear lipids from the circulation resulting in increased triglycerides KETAMINE: Ketamine causes hyperglycemia, mediated via α2-adrenoceptors agonistic action INHALATIONAL ANAESTHETIC AGENTS Inhalational anaesthetic agents leads to impaired glucose tolerance by two mechanisms Decreasing insulin secretion by inhibiting ATP sensitive potassium channels on cells of pancreas volatile anaesthetic agents increases hepatic gluconeogenesis leading to hyperglycemia  

49. REGIONAL ANAESTHESIA IN DIABETES ADVANTAGES DISADVANTAGES Regional anesthesia blunts the increases in catecholamines If autonomic neuropathy is present, profound hypotension may occur. Decreased chance of Aspiration, Postoperative nausea vomiting Infections may be increased (epidural abscesses are more common in diabetics) An awake patient hypoglycemia readily detectable Risk of nerve injuries and higher risk of ischemic injury due to use of adrenaline with Local anesthetics(Increased sensitivity)

50. GENERAL ANAESTHETIA IN DIABETIC PATIENTS ADVANTAGES DISADVANTAGES Fentanyl blocks the entire sympathetic nervous system and the hypothalamic pituitary axis Symptoms of hypoglycemia may be masked Better control of blood pressure in patients with autonomic neuropathy Controlled ventilation is needed as patients with autonomic neuropathy may have impaired ventilatory control Aggravated hemodynamic response to intubation Patient may have difficult airway Stiff joint syndrome Incomplete stomach emptying due to gastroparesis

51. INTRAOPERATIVE GLYCEMIC MANAGEMENT Surgical stress promotes hyperglycemia in the diabetic patients Short surgical procedures ,ambulatory surgeries < 4 hours with anticipated hemodynamic stability and minimal fluid shift is managed with subcutaneous insulin (short acting) every 2 hours with Blood glucose monitoring, 1 unit of regular insulin lowers plasma glucose by 25-30 mg/dl Long surgeries lasting 4 hours , with blood glucose exceeding 180mg/dl should be managed with IV insulin infusion Blood glucose monitoring to be done every 1 to 2 hours Preferred sample for glucose determination :Venous plasma or serum samples (arterial and capillary blood yields glucose values 7% higher than venous blood )  

52. SLIDING SCALE S/C INSULIN ADVISE ON INTRAOP AND POSTOP CARE

53. IV INSULIN INFUSION PREPARATION Regular insulin 100u/ml is added to 100 ml Normal saline to make concentration of 1unit/ml Blood glucose monitoring is done and dose is adjusted up or down as per insulin infusion algorithm The dose is calculated with following formula Insulin unit /hour = Plasma glucose mg/dl/150

54. IV INSULIN INFUSION IV INSULIN INFUSIO N ALOGRITHM

55. ALBERTI’S REGIMEN : Initial solution : 500ml 10% glucose + 10 mmol KCL + 15U Insulin infuse at 100ml/ hr Check blood glucose every 2hours,Adjust insulin in 5U steps Discontinue Insulin if blood glucose <90mg/dl Blood glucose (mg/dl) Advise <120 10U insulin (2U/h) 120-200 15U insulin(3U/h) >200 20 U insulin(4U/h)

56. VELLORE REGIMEN: ADVISE On the day of surgery ,Oral hypoglycemic agents and insulin omitted Hourly monitoring blood glucose levels is done ,and insulin dose is adjusted according to the regimen Serum potassium supplementation given if serum potassium<3.5mEq/l

57. TIGHT CONTROL REGIMEN Target Blood sugar is 80-100 mg/dl Indications :Pregnancy , cardiothoracic surgery , Neurosurgery Advantages Improve wound Healing Prevent wound infection Improve neurological outcomes Dissolve 50U of insulin in 250ml of NS and start infusion Insulin infusion rate = Blood glucose (mg/dl)/150 Insulin infusion rate = Blood glucose (mg/dl)/100 (if patient is obese , or on steroids) Risks-Hypoglycemia can occur, need meticulous monitoring of blood sugar

58. FLUID MANAGEMENT IN DIABETES MELITUS RINGERS LACTATE Lactate undergoes gluconeogenesis in liver and may complicate blood sugar control In patients with liver failure lactate metabolism is impaired can lead to lactic acidosis NORMAL SALINE Normal saline can be used in diabetes mellitus but Infusion of large volumes of Normal saline Can result in Hyperchloremic metabolic acidosis There is no ideal solution either solution must be used judiciously

59. MANAGEMENT OF INTRAOP HYPOGLYCEMIA Hypoglycemia- Blood glucose <60mg/dl Discontinue insulin drip D25 IV 50ml stat Recheck Blood gas every 20 minutes , repeat after 25 minutes Restart Insulin drip once Blood Glucose >70mg/dl

60. POSTOPERTIVE PERIOD Continue the insulin glucose infusion for atleast 24 hours post operatively and until the patient is capable of resuming an adequate oral intake Monitor Blood glucose at regular intervals after shifting to oral diet

61. REFERENCES MILLERS ANAESTHESIA 10 TH EDITION TATA MEMORIAL OBJECTIVES OF ANAESTHESIA

62. THANK YOU.

63. PREOPERATIVE RECOMENDATION Insulin dosing depend on 1.Type of insulin 2.Timing of dosing Subcutaneous insulin – NPH insulin reduced to 2/3 rd dose at night and half of NPH On the morning of the surgery and withheld morning dose of regular insulin Insulin pump – overnight rate decreased by 30%,and in morning of the surgery infusion is continued At the basal rate (weight in kg 24 =units/hour) Glarginine + lispro/ aspart – Reduce 2/3 rd of glarginine and entire lispro/ aspart dose night before surgery reduced