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Periop management of diabetes

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  • 1. INSULIN DR.SANDEEP NMCH, NELLORE
  • 2. INSULIN  Insulin is a protein which contains two chains (A and B) linked by disulfide bridges  First protein whose sequence was identified (1955)  51 amino acids;  6-10 mg stored in the pancreas  ~ 2 mg released per day (40 units/day)/1 unit per hour  1 unit of Insulin decrease 25 to 30 mg of glucose
  • 3.  It is released from pancreatic B cells at a low basal rate and at much higher stimulated rate in response to a variety of stimuli, especially glucose.  ProInsulin -->Insulin and C-peptide  Plasma concentration of C- peptide reflects the pancreatic activity of beta cells  Symp and parasymp systems innervate beta cells  Alpha – dec  Beta and parasymp – increases basal sec of Insulin
  • 4. Insulinis destroyed in the GIT, and must be given parenterally (s.c., i.v., i.m.). Pulmonary absorption occurs and inhalation of an aerosol is a new route of administration. t1/2 is 10 min.  Degradation :- liver and kidney remove Insulin by hydrolysis of the disulfide connection between the A and B chains through Insulinase. Further degradation by proteolysis occurs.  The liver normally clears 60% of the Insulin released from the pancreas as the terminal of portal vein blood flow, with the kidney removing 35-40% of the endogenous hormone.
  • 5. THE INSULIN RECEPTOR  Receptor consists of two heterodimers, each containing an alpha subunit, which is entirely extracellular and constitues the recongition site, and a beta subunit, which spans the membrane.  The beta subunit contains a tyrosine kinase. When Insulin binds to alpha subunit at the outside surface of the cells, tyrosine kinase activity is stimulated in the beta portion  Self-phosphorylation of the beta portion results in translocation of certain proteins such as glucose transporter from sequestered sites within adipocytes and muscle cells to exposed locations on the cell surface. Finally, the Insulin- receptor complex is internalised.
  • 6. INSULIN RECEPTOR Binding sites Cell membrane Tyrosin kinase Intracellular space Schematic diagram of the two-phase release of Insulin in response to a constant glucose infusion.
  • 7. CASCADE OF INSULIN STIMULATION Translocation of Glut 4 transpoters to plasma membranes, where by  Facilitate glucose diffusion into the cells  Facilitates glycogenisis  Stimulates cellular uptake of aminoacids, Phoshates, K+, Mg2+.  Stimulates protein synthesis and inhibits proteolysis  Regultes gene expression via Insulin regulatory elements in target DNA.
  • 8. EFFECTS OF INSULIN ON ITS TARGETS 1.Action of Insulin on glucose transporters  It has an important effect on several transport molecules that facilitate glucose movement across cell membranes (GLUT 1-GLUT 4)  GLUT-4 (inserted into the membranes of muscle and adipose cells) is responsible for Insulin- mediated uptake of glucose  GLUT-2 (B-cells of pancreas) mediates transport of glucose into pancreatic B-cells. Its defects may contribute to the reduced Insulin secretion that characterizes DM2
  • 9. Effects on liver  Anabolic  Promotes glycogenesis  Increases synthesis of triglycerides, cholesterol, and VLDL  Increases protein synthesis  Promotes glycolysis  Anticatabolic  Inhibits glycogenolysis  Inhibits ketogenesis  Inhibits gluconeogenesis Effects on muscle  Promotes protein synthesis  Increases amino acid transport  Promotes glycogen synthesis  Increases glucose transport  Inhibits activity of glycogen phosphorylase Effects on fat  Promotes triglyceride storage  Induces lipoprotein lipase, making fatty acids available for absorption into fat cells  Increases glucose transport into fat cells, thus increasing availability of - glycerol phosphate for triglyceride synthesis  Inhibits intracellular lipolysis
  • 10. INSULIN PREPARATIONS AND DELIVERY:  Therapeutic Insulin used to be purified from porcine or bovine pancreas =>functionally active, but many patients developed an immune response  Today, human Insulin is produced by recombinant DNA technology  Main side effect: Hypoglycemia (requires immediate attention!)
  • 11.  The potency of Insulin is based on the ability to decrease the BG and is expressed in units.  The potency of Insulin is 22 to 26 U per mg  Insulin U-100(100U per ml) is most commonly used preparation
  • 12. INSULIN ANALOGUES  Alteration of the Insulin peptide provides an opportunity to change the absorption rate of the molecule  Eg:- Insulin lispro (ultra-short acting Insulin) and glargine ultra-long acting Insulin are the first to use
  • 13.  Normally 6 monomers units associate with Zn and form a hexamer.  Once this hexamer dissociates and form a monomer they can be absorbed.  Thus regular Insulin has a peak action of 2 to 4 hours after its s/c inj.
  • 14. TYPES  “Natural” Insulin and four modified Insulins are used clinically:  Regular (Natural) Insulin  Insulin Lispro, Aspart  Insulin Lente  NPH Insulin  Insulin Glargine
  • 15. CLASSIFICATION  Rapid-acting - Humalog ®, Novolog ®  Short-acting - Regular  Intermediate - Lente, NPH  Long-acting - Ultralente, Glargine (Lantus)
  • 16. REGULAR (NATURAL) INSULIN  Unmodified human Insulin  Rapid acting with short duration (half-life 9 min)  Only one that can be given IV (infusions, since injections are too brief acting)  Useful for emergencies (hyperglycemic coma)
  • 17. INSULIN LISPRO  Ultra-short acting Insulin-  Monomeric Insulin produced by recombinant technology, in which two aminoacids (proline and lysine) have been reversed in their position 28 and 29 of beta chain without any influence on receptor binding.  The advantage is rapid absorption. Peak serum value is reached in 1 hr. Its use is associated with significantly improved post-glycemic control (without increasee incidence of hypoglycemia).  Used for emergency (ketoacidosis), for rapid response (surgery).
  • 18. INSULIN LENTE  Mixed with zinc => forms micro-precipitates =>Takes longer to absorb => longer acting  Only for s.c. Administration  It is a mixture of 30% semilente - an amorphous precipitate of Insulin with zinc ions in acetate buffer that has a relatively rapid onset of action + 70% of ultralente Insulin
  • 19. ULTRALENTE INSULIN  A poorly soluble crystal zinc Insulin that has a delayed onset and prolonged duration of action.  This is needed in typeI patients to achieve basal Insulin concentratin throughout the 24 hrs that are comparable to those achieved in normal subjects by basal endogenous secretion.
  • 20. NEPHAN INSULIN  Regular Insulin mixed with Protamine (0.005mg/U) (large positively charged protein)  (NPH, neutral protamine Hagedorn or isophane Insulin) is an intermediate Insulin with the delayed onset of action achieved by combining appropriate amount of Insulin and protamine.
  • 21. INSULIN GLARGINE (LANTUS®)  Amino acid asparagine at position A21 is replaced by glycine and two arginines are added to the C-terminus of the B-chain  After injection into the subcutaneous tissue, the acidic solution is neutralized, leading to formation of microprecipitates from which small amounts of Insulin Glargine are slowly released, resulting in a relatively constant concentration/time profile over 24 hours with no pronounced peak.
  • 22. Glargine
  • 23. 24 Time Activity of Human Insulins
  • 24. INSULINS NPH Lente Ultralente Onset (hr) 0.5-1 1-2 3-4 Maximum (hr) 2-3 4-10 10-15 Duration (hr) 6-8 12-18 18-26 ANALOGUES Onset (min/hr) Maximum (hr) Duration (hr) Lispro glargine 0.15-15 (min) 3-4 (hr) 0.5-1 missing 3-5 30
  • 25. INSULIN ADMINISTRATION: • Subcutaneously (oral application impossible due to degradation) • Only Regular Insulin can be given IV if needed • Jet injectors • Pen injectors • Implantable Insulin pumps • Intranasal Insulin - mucosal atrophy (abandoned) • Pulmonary Insulin (inhalation) - in clinical trial
  • 26. GLYCEMIC GOALS  Type I DM-  Before meals- 70 to 120 mg/dl  After meals- <150mg/dl  Bed time- 100 to 130 mg/dl  3 A.M- >70 mg/dl  Type II DM-  FBS & PPBS- 90-130mg/dl  Peak PPBS - <180 mg/dl  HbA1C -<7%
  • 27. 50 150 6 9 12 3 6 9 12 3   Two doses: The usual dosing commonly used. Initial Insulin therapy 50 150 6 9 12 3 6 9 12 3     Four doses: Brittle diabetic patient. Pregnant mothers specially type 1. 50 150 6 9 12 3 6 9 12 3     Four doses: Brittle diabetic patient. Pregnant mothers specially type 1. Motivated patients. 50 150 6 9 12 3 6 9 12 3    Three doses: Used for active patients. Patients taking two main meals. INSULIN THERAPYConventional therapy Intensive therapy
  • 28.  HUMULIN - NPH70/REG30  NOVOLOG- ASPRAT PROT70/REG30  HUMALOG- LISPRO PROT75/REG25
  • 29. 0 10 20 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Cause: Counter regulatory hormones response to hypoglycemia at mid-night. Increase in hepatic glucose production. Insulin resistance because of the Counter regulatory hormones. Treatment: Decrease pre-supper intermediate Insulin. Defer the dose to 9 PM. Change or start pre-bed snack. SOMOGYI PHENOMENON Rebound hyperglycemia in response to hypoglycemia
  • 30. 0 10 20 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Cause: Less Insulin at bed time. More food at bed time. Not using NPH at night. Release of counterregulatory harmones Treatment: Use enough dose. Reduce bed time snack. Add NPH pre-supper. DAWN PHENOMENON Increases in BG in the morning
  • 31. COMPLICATIONS OF INSULIN THERAPY 1. Severe Hypoglycemia (< 50 mg/dl )– Life threatening Overdose of Insulin Excessive (unusual) physical exercise A meal is missed 2. Weight gain 3. Local or systemic allergic reactions (rare) 4. Lipodystrophy at injection sites 5. Insulin resistance 6. Hypokalemia
  • 32. DRUG INTERACTIONS  Drugs(harmones) that counter hypoglycemic effects-  ACTH , estrogen, glucagon  Epinephrine inhibits the secretion of Insulin and stimulates glycogenolysis  Antibiotics (tetracycline and chloramphenicol) salicylates, and phenylbutazone increases the duration of action of Insulin and may have a direct hypoglycemic effects  Hypoglycemic effect potentiated by MAOI
  • 33. ORAL HYPOGLYCEMIC AGENTS
  • 34. ORAL HYPOGLYCEMICS Pts with type II diabetes have two physiological defects: 1. Abnormal Insulin secretion 2. Resistance to Insulin action in target tissues associated with decreased number of Insulin receptors
  • 35. MODES OF ACTION  Secretogogues (sulphonylureas and biguanides)- inc Insulin availability  Biguanides – dec or inhibit excess hepatic glucose release  Glitazones – inc Insulin sensitivity  Alpha glucosidase inhibitors- dec gastric glucose absorption
  • 36. Meglitinide Analogs Sulphonylureas Thiazolindinediones Metformin (Biguanides) Alpha Glucosidase Inhibitors
  • 37. Sulfonylureas (Oral Hypoglycemic drugs) Tolbutamide Acetohexamide Tolazamide Chlorpropamide Glipizide Glyburide (Glibenclamide Glimepiride Short acting First generation Intermediate acting Long acting Long acting Short acting Second generation
  • 38. Tolbutamid short-acting Acetohexamide intermediate- acting Tolazamide intermediate- acting Chlorpropamide long- acting Absorption Well Well Slow Well Metabolism Yes Yes Yes Yes Metabolites Inactive* Active +++ ** Active ++ ** Inactive ** Half-life 4 - 5 hrs 6 – 8 hrs 7 hrs 24 – 40 hrs Duration of action Short (6 – 8 hrs) Intermediate (12 – 20 hrs) Intermediate (12 – 18 hrs) Long ( 20 – 60 hrs) Excretion Urine Urine Urine Urine FIRST GENERATION SULPHONYLUREA COMPOUNDS ** Pts with renal impairment can expect long t1/2
  • 39. Glipizide Short- acting Glibenclamide (Glyburide) Long-acting Glimepiride Long-acting Absorption Well Well Well Metabolism Yes Yes Yes Metabolites Inactive Inactive Inactive Half-life 3 – 4 hrs Less than 3 hrs 5 - 9 hrs Duration of action 10 – 16 hrs 12 – 24 hrs 12 – 24 hrs Excretion Urine Urine Urine SECOND GENERATION SULPHONYLUREA COMPOUNDS
  • 40. MECHANISM OF ACTION Closes K -ATP Channel- exocytosis of Insulin sec granules 1) Release of Insulin from β-cells 2) Reduction of serum glucagon concentration 3) Potentiation of Insulin action on target tissues SIDE EFFECTS 1) Nausea, vomiting, abdominal pain, diarrhea 2) Hypoglycaemia 3) Dilutional hyponatraemia & water intoxication (Chlorpropamide) 4) Disulfiram-like reaction with alcohol (Chlorpropamide) 5) Weight gain 6)Inhibits protective response on heart
  • 41. SIDE EFFECTS OF SULPHONYLUREAS (contd.) 6) Blood dyscrasias (not common; less than 1% of patients) - Agranulocytosis - Haemolytic anaemia - Thrombocytopenia 7) Cholestatic obstructive jaundice (uncommon) 8) Dermatitis (Mild) 9) Muscle weakness, headache, vertigo CONTRAINDICATIONS:- 1) Type 1 DM ( Insulin dependent) 2) Parenchymal disease of the liver or kidney 3) Pregnancy, lactation 4) Major stress
  • 42. MEGLITINIDES (Repaglinide, Nateglinide) PK: Rapidly absorbed ( Peak in1hr ), Metabolized by liver t1/2 = 1 hr, Duration of action 4-5 hr MECHANISM OF ACTION Bind to the same KATP Channel to cause Insulin release from β-cells.
  • 43. MEGLITINIDES (Contd.) CLINICAL USE Approved as monotherapy and in combination with metformin in type 2 diabetes Taken before each meal, 3 times / day Does not offer any advantage over sulfonylureas; Advantage: Pts. allergic to sulfur or sulfonylurea SIDE EFFECTS: Hypoglycemia Wt gain ( less than SUs ) Caution in pts with renal & hepatic impairment.
  • 44. BIGUANIDES(Metformin) PK:- Does Not bind to plasma proteins, Not metabolized Excreted unchanged in urine t 1/2 2 hr MOA:- 1. Increase peripheral glucose utilization 2. Inhibits gluconeogenesis 3. Impaired absorption of glucose from the gut 4. Dec plasma TG & LDL & CH
  • 45. Advantages of Metformin over SUs Does not cause hypoglycemia Does not result in wt gain ( Ideal for obese pts ) SIDE EFFECTS  1. Metallic taste in the mouth  2. Gastrointestinal (anorexia, nausea, vomiting, diarrhea, abdominal discomfort)  3. Vitamin B 12 deficiency (prolonged use)  4. Lactic acidosis
  • 46. 1. Hepatic impairment 2. Renal impairment 3. Alcoholism 4. Heart failure BIGUANIDES (Contd.) CONTRAINDICATIONS 1. Obese patients with type II diabetes 2. Alone or in combination with sulfonylureas INDICATIONS
  • 47. α-GLUCOSIDASE INHIBITORS (Acarbose) Pk:- Not absorbed from intestine except small amount t1/2 3 - 7 hr Excreted with stool MOA:- Inhibits intestinal alpha-glucosidases and delays carbohydrate absorption, reducing postprandial increase in blood glucose
  • 48. α-GLUCOSIDASE INHIBITORS (Contd.) MECHANISM OF ACTION
  • 49. SIDE EFFECTS Flatulence Loose stool or diarrhea Abdominal pain Alone does not cause hypoglycemia INDICATIONS α-GLUCOSIDASE INHIBITORS Patients with Type II inadequately controlled by diet with or without other agents( SU, Metformin) Can be combined with Insulin May be helpful in obese Type II patients (similar to Metformin)
  • 50. THIAZOLIDINEDIONE DERIVATIVES (Rosiglitazone, Pioglitazone) PK:- - 99% absorbed, Metabolized by liver - 99% of drug binds to plasma proteins - Half-life 3 – 4 h, Eliminated via the urine 64% and feces 23% MOA:- - Increase target tissue sensitivity to Insulin by: reducing hepatic glucose output & increase glucose uptake & oxidation in muscles & adipose tissues. They do not cause hypoglycemia (similar to metformin and acarbose )
  • 51. ADVERSE EFFECTS - Mild to moderate edema - Wt gain - Headache - Myalgia - Hepatotoxicity THIAZOLIDINEDIONE DERIVATIVES INDICATIONS Type II diabetes alone or in combination with metformin or sulfonylurea or Insulin in patients resistant to Insulin treatment.
  • 52. WHAT ARE THE INCRETINS  GIP: Glucose-dependent Insulinotrophic polypeptide Small effect in Type 2 diabetes.  GLP-1(glucagon-like peptide 1) augmented in the presence of hyperglycaemia. Action less at euglycaemia and in normal subjects.  Pituitary Adenylate Cyclase Activating Peptide (PACAP)
  • 53. GLP-1 LOCALISATION  Cleaved from proglucagon in intestinal L-cells (and neurons in hindbrain / hypothalamus)  Secreted in response to meal ingestion  Cleared via the kidneys  GLP-1 is short-acting  t½=2.6 minutes  Native GLP-1 is rapidly degraded by DPP-IV
  • 54. Dipeptyl- peptidase inhibitors Sitagliptin Vildagliptin Saxagliptin Septagliptin Allogliptin
  • 55. SITAGLIPTIN •1st approved member of a new class of OAHA - DPP-4 inhibitor •Potent, highly selective, reversible and competitive inhibitor of DPP-4 enzyme •Tmax (median): 1 to 4 hours postdose •Apparent t½ (mean): 12.4 hours
  • 56. MECHANISM OF ACTION OF SITAGLIPTIN Incretin hormones GLP-1 and GIP are released by the intestine throughout the day, and their levels increase in response to a meal. Concentrations of the active intact hormones are increased by sitagliptin, thereby increasing and prolonging the actions of these hormones. Release of active incretins GLP-1 and GIP  Blood glucose in fasting and postprandial states Ingestion of food  Glucagon (GLP-1)  Hepatic glucose production GI tract DPP-4 enzyme Inactive GLP-1 XSitagliptin (DPP-4 inhibitor)  Insulin (GLP-1 and GIP) Glucose- dependent Glucose dependent Pancreas Inactive GIP β cells α cells  Glucose uptake by peripheral tissues 30
  • 57. ANAESTHETIC MANAGEMENT The main aims of perioperative diabetic management are to:  avoid hypoglycaemia/hyperglycaemia  aim for prompt return to oral intake  avoid dehydration  avoid hypokalaemia  prevent ketoacidosis.
  • 58. METABOLIC EFFECTS OF SURGERY:  The normal stress response to surgery affects the patient‟s Insulin requirements and depends on the nature and length of surgery.  Increased production of catabolic hormones (e.g. catecholamines, cortisol, growth hormone, thyroid hormones) and a decrease in the production and action of Insulin
  • 59. THE NATURE OF INSULIN REGIMEN DEPENDS ON  Glycemic state and goals  Nature and severity of surgery  Minor  Major  Emergency  Presence or absence of complications
  • 60. PRE -OP  Night before surgery- two thirds of total night dose  Morning of sugery - NPH/2 of usual dose and full dose of regular Insulin  Start 5%D with 0.45% of NS i.v at 1.5 ml/kg/hr (100ml/hr)  If infusion is going on – BG/150 U iv and D5W @ 1 ml/kg/hr
  • 61. PRE -OP  If patient is on Insulin pump  Over night rate- 70% of basal rate  Morning-  continue same rate as usual Stop continuous Insulin infusion s/c Glargine and discontinue pump in 60 to 90 min
  • 62. PRE -OP If patient is on Glargine and aspart  Night 2/3rd of Glargine Entire aspart/lispro  Morning Stop all
  • 63. PRE-OP If patient is on OHA  Stop Sulfonylureas It blocks myocardial K-ATP channel and inhibit ischemic preconditioning , a cardioprotective mechanism. So it should be stopped 24 to 48 hrs prior to surgery.
  • 64. PRE-OP  If for minor surgery and well controlled DM -2 – no need of Insulin  If poorly controlled type 2 DM, all type I minor surg and major surg- needs Insulin  Major surg with  BG >270mg/dl –delay surgery with rapid control  If 400 mg/dl – surgery postponed and metabolic state reestablished.
  • 65. PATIENTS UNDERGOING MINOR SURGERY:  Type 1 diabetes  First on morning list.  Insulin adjustments  If blood glucose is 12 mmol/litre (200mg/dl) or more start Insulin/dextrose/potassium regimen.  Take blood glucose measurements 1 hour preoperatively, hourly intraoperatively, and 2 hourly postoperatively until the patient is eating and drinking.  The normal Insulin regimen can be given once the patient is eating and drinking.
  • 66. MINOR SURGERY  Type 2 diabetes  Omit oral hypoglycaemic on morning of surgery except metformin, omitted much before.  Measure blood glucose as above.  Restart oral hypoglycaemics with first meal.
  • 67. PATIENTS UNDERGOING MAJOR SURGERY:  Major surgery is that not falling into the above category and emergency surgery. Type 1 and type 2 diabetes are treated the same.  Insulin managment  Start Insulin/dextrose/potassium regimen according to blood glucose.  Measure blood glucose 2 hourly during infusion and hourly during surgery.
  • 68. INTRA-OP  Avoid hyperglycemia and hypoglycemia  Ideally  Start continuous Insulin infusion 2hrs prior to surgery  If BG > 200 to 250 no use of s/c Insulin  Maintain BG 120 to 180 mg/dl
  • 69. INTRA OP  Typical rate is 0.02U/kg/hr or 1.4 U/hr in 70 kg individual  If CABG- 0.06mg/kg/hr  If on steroids /severe infection-0.04 U/kg/hr  If pt on hyperalimentation / vasopressor infusion –D51/2 NS with 20 mEqKCl at 100 to 150 ml/hr  Monitor glucose hourly& every 30 min if pt underwent CABG
  • 70. If BG(mg/dl)  <100 – D51/2 NS 150ml/hr  101-150 – 75 ml/hr  151-200 - 50 ml/hr  >200 – keep vein open
  • 71. INSULIN/DEXTROSE REGIMENS:  The two widely used regimens are the  Insulin sliding scale and  The „Alberti‟ regimen.
  • 72. INSULIN SLIDING SCALE  Insulin sliding scale uses 50 U of soluble Insulin diluted up to 50 ml with normal saline and run at a rate according to the patient‟s blood glucose.  Dextrose and potassium also need to be infused concurrently (e.g. 500 ml of 10% dextrose plus 10 mmol potassium chloride at 100 ml/hour).
  • 73. SLIDING SCALE Blood sugar mg/dl Regular Insulin 150-200 2U 200-250 4U 250-300 6U 300-350 8U Above 350 10U
  • 74. SLIDING SCALE  The amount of Insulin administered can be altered easily without having to make up a new mixture.  Risk of a failure to administer dextrose due to blockage, disconnection or backflow. Advantage Disadvantage
  • 75. THE ALBERTI REGIMEN  Combines Insulin, dextrose and potassium to remove the risk of accidental Insulin infusion without dextrose.  The amount of Insulin added to each bag depends on the patient‟s blood glucose level, so new mixtures of Insulin and dextrose have to be made up each time a change in Insulin dose is required.
  • 76. •Glucose – Potassium – Insulin infusion • Alberti and Thomas regimen (1979) To commence on the morning of surgery: 500ml 10% glucose + 10U Insulin + 1o mmol Kcl @ 100ml / hr Blood sugar every 2-3hrs Blood sugar <5mmol / L (90mg/dl) Insulin ↓ to 5u Blood sugar >10mmol / L (180- 270mg/dl) Insulin ↑ to 15
  • 77.  Combines Insulin, dextrose and potassium to remove the risk of accidental Insulin infusion without dextrose.  Costly and inefficient because it may have to be done every hour in some patients. Advantage Disadvantage
  • 78. Modified alberti regimen GIK sol 500ml of 10%dextrose + 10mmols/L of KCL +15 U Insulin @ 100ml/hr Cont new GIK sol at adjusted conc Inc Insulin by 5 U Dec Insulin by 5 U Measure BG every 2 hrs BG<120mg/ dl BG >200mg/dl BG 120-200mg continue @ same rate
  • 79. HIRSCH REGIMEN
  • 80.  Classic "Non-Tight Control" Regimen Aim:  To prevent hypoglycemia, ketoacidosis, and hyperosmolar states. protocol:  1. On the day before surgery, the patient should be kept NPO after midnight.  2. At 6 AM on the day of surgery, infuse a solution of IV fluids containing 5% dextrose at a rate of 125 mL/hr/70 kg body weight.  3. After starting the IV infusion, give half the usual morning Insulin dose (and the usual type of Insulin) subcutaneously.  4. Continue 5% dextrose solutions through the operative period and give at least 125 mL/hr/70kg body weight.  5. In the recovery room, monitor blood glucose concentrations and treat on a sliding scale
  • 81. Tight Control" Regimen 1 :- Aim:  To keep plasma glucose levels at 79 to 120 mg/dL. protocol:  1. On the evening before surgery, determine the preprandial blood glucose level.  2. begin an IVinfusion of 5% dextrose at a rate of 50 mL/hr/70 kg body weight.  3. "Piggyback" an infusion of regular Insulin (50 U in 250 mL of 0.9% sodium chloride) to the dextrose infusion with an infusion pump). Before attaching this piggyback line to the dextrose infusion, flush the line with 60 mL of infusion mixture and discard the flushing solution. This approach saturates Insulin binding sites on the tubing.  4. infusion rate: Insulin (U/hr) = plasma glucose(mg/dL)/150. (Note: The denominator should be 100 if the patient is taking corticosteroids.
  • 82. 6. On the day of surgery, intraoperative fluids and electrolytes are managed by continued administration of non-dextrose- containing solutions, as described in steps 3 and 4. 7. Determine the plasma glucose level at the start of surgery and every 1 to 2 hours for the rest of the 24-hour period. Adjust the Insulin dosage appropriately. 5. 4th hourly measure blood glucose and adjust Insulin appropriately to obtain blood glucose levels of 100 to 200 mg/dL.
  • 83. TIGHT CONTROL" REGIMEN 2 :- Aim:- same as for TCR-1 Protocol:-  obtain feedback mechanical pancreas & set controls for the desired plasma glucose regimen  institute 2 IV lines
  • 84. POST-OP  Measure blood glucose hourly for 4 hours postoperatively or until stable, whichever is longer, and then 2 hourly.  For type I patients stop the infusion once they are eating and drinking.  Calculate the total dose of Insulin in the last 24 hours and divide it into three daily doses and administer this as subcutaneous soluble Insulin.  Adjust the dose until the patient is stable, aiming to return to their normal regimen.  For type 2 patients, stop the infusion and restart oral hypoglycaemics once they are eating and drinking.
  • 85. EMERGENCY SURGERY  Patient will be in DKA/HHS  Large volume of NS and Insulin is given  Insulin  Bolus – 0.1u/kg  Infusion-0.1u/kg/hr  Check – BG hrly and electrolytes 2nd hrly  If BG <250 – add dextrose  Continue infusion till acidosis decreases
  • 86. IMPORTANT POINTS TO BE NOTED WHILE GIVING INSULIN 1. Absorption of Insulin is highly variable (type, species, site and blood flow ) 2. 1 U of Insulin = 25-30 mg% 3. Daycare patients should have preceeding evening Insulin reduced by 10-20% to prevent hypoglycemia early morning
  • 87. 4. Insulin sliding scales have no benefit in poorly controlled surgical patients 5. Intravenous Insulin is the most precise means of managing hyperglycemia perioperatively and several regimes are recommended 6. Interruption of Insulin infusion suddenly leads to sudden metabolic decompensation 7. Insulin is adsorbed to glassware as well as plastic ware. (around 30%)
  • 88. • Measures to decrease loss a) Running about 50 ml of infusate rapidly through the tubing to saturate the sites b) Add small amount of protein to the infusate 8. Higher Insulin dose required in case of administration of RL during surgery
  • 89. MISC……. • BZD‟s – if given by continous infusion, decreases blood glucose ( by decreasing the ACTH, decreases cortisol ) • High dose opiate – abolish hyperglycemia by blocking sympathetic response • Halothane, Enflurane and Isoflurane in vitro, inhibit the Insulin response to glucose in a reversible and dose dependent manner.  General medical/surgical Fasting : 90-126 mg% Random: < 200 mg%  Cardiac surgery < 150 mg%  Critically ill < 150 mg%  Acute neurologic disorders 80 – 140 mg%
  • 90. REFERENCES  Anaesthetic management of the diabetic patient. Simon Webster Nicola Lewis, ANAESTHESIA AND INTENSIVE CARE MEDICINE, 2005  Harrison‟s principles of Internal medicine, 17th edition  Miller‟s Anesthesia 6th edition.  Stoelting‟s anesthesia & coexisting diseases, 4th & 5th edition  ISACON 2007, CME lectures.  Morgan anesthesia
  • 91. THANK YOU

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