Diabetes Mellitus


Published on

  • Njce! Thanks for sharing.
    Are you sure you want to  Yes  No
    Your message goes here
  • Diabetes Symptoms

    The signs are:

    a) Tiredness in light of the way that you can make use of your glucose

    b) High circulatory strain

    c) Pulse rate high

    d) Wound that takes long time to retouch.

    There are 2 sort of diabetes –

    Sort 1 Diabetes :

    a)your body can make glucose and insulin need to be implanted.

    Sort 2 Diabetes: Your body can convey glucose however can't make use of it. So your sugar level gets high. You oblige some instrument to open up the cell to let the glucose dissimulate. The effect of whole deal diabetes:

    a) stroke,

    b) your may confined your foot

    c) confined you place

    d) kidney if the sugar level is not controlled.

    You can controlled diabetes however not cure at this moment, so charge thee well on the off chance that you have this signs. Counsel your expert and take the drug regular
    For Detailed Consultation you can visit us on
    Are you sure you want to  Yes  No
    Your message goes here
  • I salute your hard work, thanks for this diabetes document. I found this one on internet.. this may help some diabetes patients in Hyderabad : https://www.facebook.com/DiabetologistHyderabad, they are providing the best diabetes treatment in India
    Are you sure you want to  Yes  No
    Your message goes here
No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Diabetes Mellitus

  1. 1. Perioperative Management of Diabetes Mellitus Amir B. Channa FFARCS, D.A. (Eng) KKUH - Riyadh
  2. 2. <ul><li>The global incidence of diabetes is rising and the number of people affected is projected to exceed 300 million by the year 2025 </li></ul><ul><li>Type 2 diabetes affects over 90% of diabetics </li></ul><ul><li>25% of world population obese – dramatic rise in incidence of type 2 diabetes </li></ul>Introduction
  3. 3. Introduction <ul><li>Diabetes Mellitus, the most commonly encountered perioperative endocrinopathy, continuous to increase dramatically in prevalence </li></ul><ul><li>Diabetic patients commonly have microvascular and macrovascular pathology that influences their perioperative course and critical illness and increases morbidity and mortality rates during hospitalization. </li></ul>
  4. 4. Introduction <ul><li>Since diabetics require more surgeries than their nondiabetic counterparts, </li></ul><ul><ul><li>preemptive identification and </li></ul></ul><ul><ul><li>anticipation of diabetic complications </li></ul></ul><ul><ul><li>and comorbidities, </li></ul></ul><ul><ul><li>along with an optimized treatment plan, are the foundation for the proper care of this growing patient population </li></ul></ul>
  5. 5. Introduction <ul><li>Aggressive glycemic management improves short- and long-term outcomes in diabetic patients with acute myocardial infarction and cardiac surgical patients. </li></ul><ul><li>Recently is has been shown that tight glycemic control in both diabetic and nondiabetic hyperglycemic intensive care patients resulted in improved survival </li></ul><ul><li>Blood glucose readings > 12.2 mmol/l on the first post-op day are associated with a 2.7 fold increased risk of infection </li></ul>
  6. 6. Epidemiology <ul><li>Estimated 245 million people globally </li></ul><ul><li>20%of adult population </li></ul><ul><li>5% of all deaths each year </li></ul><ul><li>80% of people with diabetes live in low and middle income countries </li></ul>
  7. 7. Patients with diabetes: what pre-operative assessment is important? <ul><li>Document the following </li></ul><ul><ul><li>Type of diabetes </li></ul></ul><ul><ul><li>L ength of time since diagnosis </li></ul></ul><ul><ul><li>Current management </li></ul></ul><ul><ul><li>Current glycemic control </li></ul></ul><ul><ul><ul><li>HgBA1c </li></ul></ul></ul><ul><ul><ul><li>Glucometer data </li></ul></ul></ul><ul><ul><li>Presence of complications </li></ul></ul><ul><ul><ul><li>Neuropathy </li></ul></ul></ul><ul><ul><ul><li>Nephropathy </li></ul></ul></ul><ul><ul><ul><li>Retinopathy </li></ul></ul></ul>Autonomic neuropathy increase risk of post op gastroparesis and urinary tract infection
  8. 8. Diabetic Acute Complications (1) Diabetic ketoacidosis. (2) (Hyperglycemic) hyperosmolarity non-ketotic states. (3) Hypoglycemia. Diabetic Chronic Complications (i) Macro-angiopathy (4) Cerebrovascular disease (5) Coronary heart disease: Asymptomatic ischemia (6) Peripheral vascular disease (ii) Micro-angiopathy (7) Retinopathy (8) Nephropathy (9) Neuropahthy Peripheral neuropathy Autonomic neuropathy (iii) (10) Diabetic foot infection
  9. 9. Long-term Complications of Diabetes Mellitus <ul><li>Blindness </li></ul><ul><ul><li>Retinal hemorrhages </li></ul></ul><ul><li>Renal Disease </li></ul><ul><li>Peripheral Neuropathy </li></ul><ul><ul><li>Numbness in “stocking glove” distribution (hands and feet) </li></ul></ul><ul><li>Heart Disease and Stroke </li></ul><ul><ul><li>Chronic state of Hyperglycemia leads to early atherosclerosis </li></ul></ul><ul><li>Complications in Pregnancy </li></ul>
  10. 10. Long-term Complications of Diabetes Mellitus <ul><li>Diffuse Atherosclerois </li></ul><ul><ul><li>AMI </li></ul></ul><ul><ul><li>CVA </li></ul></ul><ul><ul><li>PVD </li></ul></ul><ul><ul><ul><li>Hypertension </li></ul></ul></ul><ul><ul><li>Renal failure </li></ul></ul><ul><ul><li>Diabetic retinopathy/blindness </li></ul></ul><ul><ul><li>Gangrene </li></ul></ul>
  11. 11. Long-term Complications of Diabetes Mellitus 10% of all diabetics develop renal disease usually resulting in dialysis Diabetics are up to 4 times more likely to have heart disease and up to 6 times more likely to have a stroke than a non-diabetic
  12. 12. Long-term Complications of Diabetes Mellitus <ul><li>Peripheral Neuropathy </li></ul><ul><ul><li>Silent MI </li></ul></ul><ul><ul><ul><li>Vague, poorly-defined symptom complex </li></ul></ul></ul><ul><ul><ul><ul><li>Weakness </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Dizziness </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Malaise </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Confusion </li></ul></ul></ul></ul><ul><ul><ul><li>Suspect MI in any diabetic with MI signs/symptoms with or without CP </li></ul></ul></ul>
  13. 13. Why is pre-op glycemic control important? <ul><li>Poor glycemic control </li></ul><ul><ul><li>Increases dehydration and electrolyte abnormalities </li></ul></ul><ul><ul><li>Impairs collagen formation and decreases surgical wound strength </li></ul></ul><ul><ul><li>Increases risk of complications </li></ul></ul><ul><li>Medications for diabetes management associated with risks </li></ul>
  14. 14. Diagnosis <ul><li>Symptoms of diabetes + random plasma glucose > 11.1 mmol/l </li></ul><ul><li>Fasting plasma glucose >7.0 mmol/l </li></ul><ul><li>2 hour Plasma glucose >11.1 mmol/l during a standard 75g glucose tolerance test </li></ul>
  15. 15. Regulation of Glucose Insulin Glucagon Glucagon and Insulin are opposites (antagonists) of each other.
  16. 16. Endocrine Effects of Insulin <ul><li>Effects on Liver </li></ul><ul><ul><li>Anabolic </li></ul></ul><ul><ul><ul><li>Promotes glycogensis </li></ul></ul></ul><ul><ul><ul><li>Increases synthesis of triglycerides, cholesterol and VLDL </li></ul></ul></ul><ul><ul><ul><li>Increases protein synthesis </li></ul></ul></ul><ul><ul><ul><li>Promotes glycoysis </li></ul></ul></ul><ul><ul><li>Anticatabolic </li></ul></ul><ul><ul><ul><li>Inhibits gylogensis </li></ul></ul></ul><ul><ul><ul><li>Inhibits ketogensis </li></ul></ul></ul><ul><ul><ul><li>Inhibits gluconeogensis </li></ul></ul></ul><ul><ul><ul><li>ss </li></ul></ul></ul>
  17. 17. Endocrine Effects of Insulin <ul><li>Effects on Muscle </li></ul><ul><ul><li>Promotes protein synthesis </li></ul></ul><ul><ul><ul><li>Increases amino acid transport </li></ul></ul></ul><ul><ul><ul><li>Stimulates ribosomal protein synthesis </li></ul></ul></ul><ul><ul><li>Promotes glycogen synthesis </li></ul></ul><ul><ul><ul><li>Increases glucose transport </li></ul></ul></ul><ul><ul><ul><li>Enhances activity of glycogen sythetase </li></ul></ul></ul><ul><ul><ul><li>Inhibits activity of glycogen phosphorylase </li></ul></ul></ul>
  18. 18. Endocrine Effects of Insulin <ul><li>Effects on Fat </li></ul><ul><ul><li>Promotes triglyceride storage </li></ul></ul><ul><ul><ul><li>Induces lipoprotein lipase, making fatty acids available for absorption into fat cells </li></ul></ul></ul><ul><ul><li>Increases glucose transport into fat cells, thus increases availability of  -glycerol phosphate for triglyceride synthesis </li></ul></ul><ul><ul><li>Inhibits intracellular lipolysis </li></ul></ul>
  19. 19. Etiological Classification <ul><li>Type I diabetes: Pancreatic β-cell destruction, usually leading to absolute insulin deficiency </li></ul><ul><ul><li>Immune mediated </li></ul></ul><ul><ul><li>Idiopathic </li></ul></ul>
  20. 20. Etiological Classification <ul><li>Type I diabetes </li></ul><ul><li>Type 2 diabetes: Defective insulin secretion and usually insulin resistance </li></ul>
  21. 21. Etiological Classification <ul><li>Type I diabetes </li></ul><ul><li>Type 2 diabetes </li></ul><ul><li>Other specific types </li></ul><ul><li>a. Genetic defects of β-cell function </li></ul><ul><li>b. Genetic defects of insulin action </li></ul><ul><li>c. Diseases of the exocrine pancreas </li></ul><ul><li>d. Endocrinopathies ( pheo.cushing,cortico steroids,acromegaly) </li></ul><ul><li>e. Drug (thiazides) or chemical induced </li></ul><ul><li>f. Infections </li></ul><ul><li>g. Associated genetic defects </li></ul><ul><li>h. Uncommon auto-immune causes </li></ul>
  22. 22. Etiological Classification <ul><li>Type I diabetes </li></ul><ul><li>Type 2 diabetes </li></ul><ul><li>Other specific types </li></ul><ul><li>4. Gestational diabetes: Onset in, or first diagnosed in pregnancy </li></ul>
  23. 23. Acute effects of hyperglycaemia <ul><li>Dehydration and electrolyte disturbances (due to osmotic diuresis) </li></ul><ul><li>Acidaemia (accumulation of lactic + ketoacids) </li></ul><ul><li>Fatigue, weight loss and muscle wasting (lipolysis and proteolysis in absolute insulin deficiency) </li></ul><ul><li>Poor wound healing and impaired wound strength </li></ul><ul><li>Diabetic ketoacidotic coma (Type I diabetics due to absolute insulin deficiency) </li></ul><ul><li>Hyperosmolar Non-ketotic coma (Type II diabetics) </li></ul>
  24. 24. Chronic effects of Hyperglycaemia <ul><li>Microvascular </li></ul><ul><ul><li>Proliferative retinopathy </li></ul></ul><ul><ul><li>Diabetic nephropathy (close association with hypertension, which is found in 30-60% of diabetics) </li></ul></ul>
  25. 25. <ul><li>Microvascular </li></ul><ul><li>Macrovascular </li></ul><ul><ul><li>Atherosclerosis </li></ul></ul><ul><ul><ul><li>Coronary heart disease (beware silent ischaemia, cardiomyopathy) </li></ul></ul></ul><ul><ul><ul><li>Cerebrovascular disease </li></ul></ul></ul><ul><ul><ul><li>Peripheral vascular disease </li></ul></ul></ul>
  26. 26. <ul><li>Microvascular </li></ul><ul><li>Macrovascular </li></ul><ul><li>Neuropathic </li></ul><ul><ul><li>Peripheral </li></ul></ul><ul><ul><ul><li>Motor (Mononeuropathies, pressure palsies) </li></ul></ul></ul><ul><ul><ul><li>Sensory polyneuropathy </li></ul></ul></ul>
  27. 27. Microvascular <ul><li>Microvascular </li></ul><ul><li>Macrovascular </li></ul><ul><li>Neuropathic </li></ul><ul><ul><li>Peripheral </li></ul></ul><ul><ul><li>Autonomic </li></ul></ul><ul><ul><ul><li>Diarrhea </li></ul></ul></ul><ul><ul><ul><li>Urinary incontinence </li></ul></ul></ul><ul><ul><ul><li>Postural hypotension </li></ul></ul></ul><ul><ul><ul><li>Cardiac denervation </li></ul></ul></ul><ul><ul><ul><li>Impaired ventilatory control – risk of resp arrest with anaesthesia </li></ul></ul></ul><ul><ul><ul><li>Gastroparesis </li></ul></ul></ul>
  28. 28. <ul><li>Microvascular </li></ul><ul><li>Macrovascular </li></ul><ul><li>Neuropathic </li></ul><ul><li>“ Stiff joint syndrome” (airway) </li></ul><ul><li>Increased incidence of infections </li></ul>
  29. 29. Autonomic Neuropathy <ul><li>Orthostatic hypotension </li></ul><ul><li>Resting tachycardia </li></ul><ul><li>Gastroparesis(vomiting,diarrhea) </li></ul><ul><li>Impotence </li></ul><ul><li>Cardiac dysrhythmias </li></ul><ul><li>Asymptomatic hypoglycemia </li></ul><ul><li>Sudden death syndrome </li></ul>
  30. 30. Autonomic Neuropathy <ul><li>Orthostatic hypotension </li></ul><ul><li>Resting tachycardia </li></ul><ul><li>Gastroparesis(vomiting,diarrhea) </li></ul><ul><li>Impotence </li></ul><ul><li>Cardiac dysrhythmias </li></ul><ul><li>Asymptomatic hypoglycemia </li></ul><ul><li>Sudden death syndrome </li></ul>
  31. 31. Peri-op problems <ul><li>Stress response to surgery with catabolic hormone secretion </li></ul><ul><li>Interruption of food intake, pre- and perhaps post- surgery (also PONV) </li></ul><ul><li>Altered consciousness, masking the symptoms of hypoglycaemia </li></ul><ul><li>Circulatory disturbance that may alter the uptake of s.c. insulin </li></ul><ul><li>The altered physiological state resulting from end organ pathology </li></ul>
  32. 32. Peri-operative goal <ul><li>Minimize morbidity </li></ul><ul><li>Avoiding hyperglycaemia and its associated lipolysis, ketogenesis, protein catabolism and electrolyte disturbances </li></ul><ul><li>Avoiding hypoglycaemia </li></ul>
  33. 33. How? <ul><li>Provide adequate insulin to the patient to counteract the catabolic processes that develop in response to surgery </li></ul><ul><li>Glucose needs to be provided to meet the increased metabolic needs, caused by surgical stress, as well as basal metabolic requirements </li></ul><ul><li>A simple regimen that is immune to error </li></ul>
  34. 34. Regimen depends on <ul><li>Type of diabetes and its usual treatment </li></ul><ul><li>Extent of surgery </li></ul><ul><ul><li>The amount of surgical stress and the catabolic response to that stress </li></ul></ul><ul><ul><li>Beware major surgery and emergency surgery, especially trauma or surgery related to infective processes </li></ul></ul>
  35. 35. Type II diabetes on diet alone <ul><li>If fasting blood glucose < 7.8 mmol/l </li></ul><ul><li>Close observation including hourly dextrose measurement (glucometer in theatre) </li></ul><ul><li>Conversion to a GIK regime if the glucose rises >8.0 mmol/l </li></ul>
  36. 36. Type II diabetes on oral hypoglycaemics <ul><li>There are 4 groups of oral hypoglycaemic agents (OHA) </li></ul><ul><ul><li>Sulphonylureas </li></ul></ul><ul><ul><ul><li>Enhanced secretion of insulin in response to glucose and increased sensitivity at its peripheral actions </li></ul></ul></ul>
  37. 37. <ul><li>Sulphonylureas </li></ul><ul><li>Biguanides </li></ul><ul><ul><li>Promote glucose utilization and reduce hepatic glucose production </li></ul></ul>
  38. 38. <ul><li>Sulphonylureas </li></ul><ul><li>Biguanides </li></ul><ul><li>Thiazolidinediones (Rosiglitazone) </li></ul><ul><ul><li>Enhance insulin action in the periphery </li></ul></ul><ul><ul><li>Inhibit hepatic gluconeogenesis </li></ul></ul><ul><ul><li>Enhances glucose uptake into tissues via GLUT-4 glucose transporter </li></ul></ul><ul><ul><li>Preserves the β -cells of the pancreas </li></ul></ul>
  39. 39. <ul><li>Sulphonylureas </li></ul><ul><li>Biguanides </li></ul><ul><li>Thiazolidinediones </li></ul><ul><li>Modifiers of glucose absorption e.g.. Ά-glucosidase inhibitor acarbose </li></ul><ul><ul><li>Suppress the breakdown of complex carbohydrates in the gut delaying the rise of blood sugar postprandially </li></ul></ul>
  40. 41. ? Stop the OHA before surgery <ul><li>The long acting sulphonylureas should be stopped 3 days before surgery and converted to shorter acting drugs, or insulin if coming for major surgery </li></ul><ul><li>Metformin need not be stopped (recommendation used to be 2 days) </li></ul><ul><ul><li>Risk of lactic acidosis extremely low </li></ul></ul><ul><li>Omit morning OHA dose </li></ul>
  41. 42. <ul><li>If the patient is for minor surgery the OHA is omitted on the day of surgery and they can then be treated without insulin, with close observation and conversion to GIK if the glucose rises above 8.0 mmol/l </li></ul>
  42. 43. <ul><li>If the patient is for major surgery the patient should be established on insulin pre-op, even if well controlled. There is good evidence that continuous I.v insulin infusions are superior to intermittent s.c.boluses and also to I.v. boluses </li></ul><ul><li>GIK systems (Alberti regimen) are relatively safe as they provide insulin and dextrose together, preventing potential disasters. </li></ul>
  43. 44. Type I diabetes <ul><li>These patients should all be treated on I.v. insulin infusion before, during and after surgery. </li></ul><ul><li>This is true for major surgery, although there are some alternatives in minor surgery </li></ul>
  44. 45. Preoperative Insulin Traditional Approach <ul><li>Give 1/4 to 1/2 the daily dose of intermediate-acting insulin subcutaneously </li></ul><ul><li>Add 1/2 unit of intermediate-acting insulin for each unit of insulin prescribed </li></ul><ul><li>Start IV glucose 5-10 g/h </li></ul>
  45. 46. Preoperative Insulin Continuous IV Infusion <ul><li>Place 50 U. Regular Insulin in 1000 ml NS </li></ul><ul><li>Give 10 ml/h </li></ul><ul><li>Measure blood glucose q.h. </li></ul><ul><li>Adjust infusion rate to keep glucose level at </li></ul><ul><li>120-180 mg/dl </li></ul><ul><li>Turn infusion off for 30 min if glucose level falls below 80 mg/dl </li></ul><ul><li>Provide sufficient glucose (5-10g/h) and potassium (2-4 mEq/h) </li></ul>
  46. 47. New insulin delivery modes <ul><li>Continuous subcutaneous infusions </li></ul><ul><li>Continuous intra-peritoneal infusions </li></ul>
  47. 48. Minor surgery <ul><li>If patient is expected to resume oral intake quickly after surgery, a reduced approach may be acceptable </li></ul><ul><li>These patients will be given ½ their intermediate acting insulin, and a 5% dextrose solution at 100-150 ml/hour to prevent hypoglycaemia. </li></ul><ul><li>Intra-op and recovery room blood sugar monitoring is essential. </li></ul><ul><li>It is suggested that the blood sugar is measured every 30 mins to hourly. </li></ul>
  48. 49. Minor surgery <ul><li>Keep glucose between 4.4 – 8.0 mmol/l </li></ul><ul><li>Both I.v insulin infusions and I.v glucose may be needed to achieve control. </li></ul><ul><li>Once the patient has had their first meal post-op they can be given the rest of their insulin dose depending on the measured blood glucose </li></ul>
  49. 50. Major surgery <ul><li>Places a much larger catabolic stress on patients </li></ul><ul><li>A glucose, Potassium and insulin (GIK) infusion is a simple reliable way of controlling the patient’s blood sugar in the perioperative period </li></ul><ul><li>Ideally it should be started in the preoperative period especially in those patients that are not well controlled </li></ul><ul><li>It is essential that there are frequent, accurate measurements of the blood sugar made throughout the perioperative period </li></ul>
  50. 51. Factors that need to be considered <ul><li>Glucose </li></ul><ul><li>Insulin </li></ul><ul><li>Potassium </li></ul><ul><li>Fluids </li></ul>
  51. 52. Glucose <ul><li>Sufficient glucose is given to prevent hypoglycaemia and to provide basal energy requirements </li></ul><ul><li>It is recommended that 5-10g of dextrose is given per hour. </li></ul><ul><li>This can be given as 5% or 10% dextrose. </li></ul><ul><li>An easy way is to give 0.1g/kg/hour </li></ul>
  52. 53. <ul><li>Example: </li></ul><ul><ul><li>70kg x 0.1g/kg/hr = 7g/hr </li></ul></ul><ul><ul><li>10% dextrose contains 100mg dextrose/ml or 1g dextrose/10ml </li></ul></ul><ul><ul><li>Give 70mls/hr of 10% dextrose </li></ul></ul>
  53. 54. <ul><li>For long-term infusions 0.9% sodium chloride may be needed to prevent hyponatraemia </li></ul><ul><li>In diabetic paediatric patients, a higher dose of dextrose is probably needed and it has been estimated that 0.3g/kg/hr is sufficient to prevent hypoglycaemia </li></ul>
  54. 55. Insulin <ul><li>The β-cells in the pancreas secrete insulin in response to glucose concentrations. </li></ul><ul><li>Even the most sophisticated artificial insulin delivery systems cannot replicate this response </li></ul><ul><li>S.c. insulin will result in peaks and troughs that risk the development of lipolysis and proteolysis </li></ul><ul><li>During surgery alterations in blood flow to the skin and subcutaneous tissue makes the absorption of insulin even more unpredictable </li></ul>
  55. 56. Insulin <ul><li>Soluble rapid onset insulins are used in perioperative infusions </li></ul><ul><li>They have a short I.v. half life of about 5 min, and a biological duration of action of less than 20 min. </li></ul><ul><li>This may result ins ‘roller coaster’ effect on glucose concentrations </li></ul><ul><li>Continuous I.v. insulin infusion is the most rational way to safely control blood sugar </li></ul>
  56. 57. <ul><li>The usual requirements are 0.25-0.35 Units insulin per gram of glucose per hour. </li></ul><ul><li>Insulin requirements are increased with: </li></ul><ul><ul><li>Liver disease </li></ul></ul><ul><ul><li>Obesity </li></ul></ul><ul><ul><li>Severe infections </li></ul></ul><ul><ul><li>Steroid therapy </li></ul></ul><ul><ul><li>CPB </li></ul></ul>
  57. 58. Potassium <ul><li>Several factors affect the serum potassium level: </li></ul><ul><ul><li>Insulin stimulates the uptake of potassium into cells </li></ul></ul><ul><ul><li>Dehydration can move K+ out of the cells and into the blood </li></ul></ul><ul><ul><li>Hyperglycaemia can also move K+ out of the cells </li></ul></ul><ul><ul><li>Acid-base changes (acidosis results in hyperkalaemia </li></ul></ul>
  58. 59. <ul><li>It has been suggested that each liter of dextrose containing fluid that is used in the GIK infusion contains 40mEq KCL. </li></ul><ul><li>This can be adjusted according to plasma concentrations </li></ul><ul><li>All diabetics should have potassium measured in the operating room in addition to glucose </li></ul>
  59. 60. Fluids <ul><li>As long as the patient is receiving enough glucose, insulin and potassium any other fluids needed intraoperatively should be non-glucose containing </li></ul><ul><li>It has been suggested that lactated Ringers should not be used, as lactate is a gluconeogenic precursor that is rapidly metabolized especially in a starved or catabolic state. This may result in higher blood glucose concentrations, and should be avoided </li></ul>
  60. 61. Suggested GIK regimen <ul><li>Normal insulin the day before surgery </li></ul><ul><ul><li>Do a blood sugar on the day of surgery, and once result known start infusion </li></ul></ul><ul><ul><li>1. 1 liter 10% dextrose + 40 mEq/l KCL at 0.1g dextrose/kg/hr </li></ul></ul><ul><ul><li>2. Insulin infusion of 50 U rapid acting insulin in 250 ml 0.9% NaCl piggybacked to the dextrose and run at 1-2 U/hr depending on hourly (or more) measurements of glucose </li></ul></ul><ul><ul><li>Care should be taken that neither infusion is allowed to stop while the other continues running </li></ul></ul>
  61. 62. Insulin infusion Blood sugar Insulin 5-10 mmol/l 2 U/hr (10ml/hr) 10-13 mmol/l 4 U/hr 13-16 mmol/l 6 U/hr 16-19 mmol/l 8 U/hr >19 mmol/l 10 U/hr
  62. 63. <ul><li>The infusion should be continued post-op with hourly blood sugar monitoring </li></ul><ul><li>The patient must eat as soon as possible, and must then be put on the pre-op regimen that he was controlled on </li></ul>
  63. 64. A few anaesthetic considerations <ul><li>First case in the morning to minimize the starvation period </li></ul><ul><li>No anaesthetic technique is indicated or contraindicated in diabetics, and the stress imposed by the anaesthetic is usually minor compared to the stress of the surgery. </li></ul><ul><li>The challenge is to give the most stable anaesthetic possible and limit the hyperglycaemic reaction to surgical stress </li></ul>
  64. 65. Regional anaesthesia <ul><li>Pro: </li></ul><ul><ul><li>Regional anaesthesia blunts the increases in coritcol, glucagon, and glucose. </li></ul></ul><ul><ul><li>Spinal or epidural may modulate the catecolamine secretion, preventing high glucose and ketosis. This effect could continue in the post operative period, if the block is continued </li></ul></ul><ul><ul><li>An awake patient is a good monitor to prevent hypoglycaemia </li></ul></ul><ul><ul><li>A swifter return to normal eating </li></ul></ul>
  65. 66. Regional anaesthesia <ul><li>Con: </li></ul><ul><ul><li>If autonomic neuropathy is present, profound hypotension may occur. This could be disastrous in a patient with cardiac complications </li></ul></ul><ul><ul><li>Infections and vascular complications may be increased (epidural abscesses are more common in diabetics) </li></ul></ul><ul><ul><li>A diabetic neuropathy presenting post-op may be attributed to the regional blockade </li></ul></ul>
  66. 67. General Anaesthesia <ul><li>Pro: </li></ul><ul><ul><li>High dose opiate technique may be useful to block the entire sympathetic nervous system and the hypothalamic pituitary axis </li></ul></ul><ul><ul><li>Better control of blood pressure in patients with autonomic neuropathy </li></ul></ul>
  67. 68. General Anaesthesia <ul><li>Con </li></ul><ul><ul><li>May have difficult airway (“Stiff-joint syndrome”) </li></ul></ul><ul><ul><li>Full stomach due to gastroparesis </li></ul></ul><ul><ul><li>Controlled ventilation is needed as patients with autonomic neuropathy may have impaired ventilatory control </li></ul></ul><ul><ul><li>Aggravated haemodynamic response to intubation </li></ul></ul><ul><ul><li>Anaesthesia masks the symptoms of hypoglycaemia </li></ul></ul>
  68. 69. Summary <ul><li>The most important factors are good control of the patient’s perioperative blood glucose concentrations to prevent the acute complications of hyperglycaemia </li></ul><ul><li>The strict avoidance of any hypoglycaemia </li></ul><ul><li>The complications of diabetes should be sought out and the affected organs protected, especially the heart, brain and kidneys </li></ul><ul><li>An aggressive approach to glycaemic control will result in better wound healing, lower mortality and shorter hospital stays </li></ul>
  69. 70. Diabetes Complications
  70. 71. <ul><li>Diabetic Ketoacidosis </li></ul><ul><li>Most serious complication in Type 1 diabetes </li></ul>DKA
  71. 72. Questions??????
  72. 73. Precipitating Causes <ul><li>Not enough insulin </li></ul><ul><li>Skipping insulin </li></ul><ul><li>Stress, trauma </li></ul><ul><li>Insulin resistance </li></ul>
  73. 74. Pathophysiology of DKA <ul><li>See chart </li></ul><ul><li>Ketosis </li></ul><ul><li>Dehydration </li></ul><ul><li>Electrolyte imbalance </li></ul>
  74. 75. Complications of DKA and clues to their development <ul><li>Acute gastric dilatation or erosive gastritis </li></ul><ul><ul><li>by vomiting blood or coffee-ground material </li></ul></ul><ul><li>Cerebral edema </li></ul><ul><ul><li>obtundation or coma with or without neuro. Signs, especially if occurring with initial improvement. </li></ul></ul><ul><li>Hyperkalemia cardiac arrest </li></ul><ul><li>hypokalemia cardiac arrythmias. </li></ul><ul><li>Infection is known by fever </li></ul><ul><li>hypoglycemia is considered when there is adrenergic or neuorologic signs or rebound ketosis. </li></ul>
  75. 76. Symptoms of DKA <ul><li>Abdominal pain </li></ul><ul><li>Anorexia </li></ul><ul><li>Dehydration </li></ul><ul><li>Fuity breath </li></ul><ul><li>Kussmaul’s </li></ul><ul><li>Change LOC </li></ul><ul><li>Hypotension </li></ul><ul><li>N&V </li></ul><ul><li>Polyuria </li></ul><ul><li>Somnolence </li></ul><ul><li>Tachycardia </li></ul><ul><li>Thirst </li></ul><ul><li>Visual disturbances </li></ul><ul><li>Warm, dry skin </li></ul><ul><li>Weakness </li></ul><ul><li>Wt. loss </li></ul>
  76. 77. Assessment DKA <ul><li>Hyperglycemia </li></ul><ul><li>Hyperosmolality </li></ul><ul><li>Dehydration </li></ul><ul><li>Electrolyte imbalances </li></ul><ul><li>Metabolic acidosis </li></ul><ul><li>Hypoglycemia </li></ul><ul><li>Fluid overload </li></ul>
  77. 78. Intervention <ul><li>Rehydrate </li></ul><ul><li>Reverse shock </li></ul><ul><li>Give Potassium </li></ul><ul><li>Corret pH </li></ul><ul><li>Give insulin </li></ul>
  78. 79. Critical Monitoring <ul><li>Rehydration </li></ul><ul><ul><li>I & O, Daily Weight </li></ul></ul><ul><ul><li>Skin turgor, LOC, VS </li></ul></ul><ul><ul><li>CVP measurement </li></ul></ul><ul><ul><li>Auscultation of lungs </li></ul></ul>
  79. 80. IV Fluids in DKA <ul><li>Hour 1 </li></ul><ul><ul><li>N/S (15-20ml/kg) </li></ul></ul><ul><li>Hour 2 </li></ul><ul><ul><li>Continue fluid, consider half-strength NS </li></ul></ul><ul><li>Hour 3 </li></ul><ul><ul><li>Reduce fluid intake to 7.5ml/kg, use half-strength NS </li></ul></ul><ul><li>Hour 4 </li></ul><ul><ul><li>Consider urine output in adjusting fluids </li></ul></ul>
  80. 81. Potassium Replacement in DKA <ul><li>Look at EKG </li></ul><ul><li>Replacement is based on plasma potassium level </li></ul><ul><li>Recheck potassium q 2 hours </li></ul>
  81. 82. Correct pH/Give Insulin <ul><li>Give IV Insulin </li></ul><ul><li>Give Regular Insulin only </li></ul><ul><ul><li>Initial bolus IV (0.15u/kg) </li></ul></ul><ul><ul><li>Then Regular Insulin IV drip </li></ul></ul>
  82. 83. HHNK Hyperglycemic, Hyperosmolar Noketotic Syndrome <ul><li>Most commonly occurs in older adults with Type II diabetes </li></ul><ul><li>Always look for precipitating factors </li></ul>
  83. 84. Factors Associated with HHNK <ul><li>Drugs </li></ul><ul><li>Procedures </li></ul><ul><li>Chronic illness </li></ul><ul><li>Acute illness </li></ul>
  84. 85. Four Major Clinical Features <ul><li>Severe hyperglycemia </li></ul><ul><li>No or slight ketosis </li></ul><ul><li>Profound dehydration </li></ul><ul><li>Hyperosmolality </li></ul>
  85. 86. Treatment <ul><li>Similar to DKA </li></ul><ul><li>Find underlying cause </li></ul>
  86. 87. Hypoglycemia <ul><li>Also known as insulin reaction or hypoglycemic reaction </li></ul>
  87. 88. Risk Factors <ul><li>Overdose of insulin </li></ul><ul><li>Omitting a meal </li></ul><ul><li>Overexertion </li></ul><ul><li>Nausea and vomiting </li></ul><ul><li>Alcohol intake </li></ul>
  88. 89. Symptoms of Hypoglycemia <ul><li>Adrenergic </li></ul><ul><ul><li>Shakiness </li></ul></ul><ul><ul><li>Irritability </li></ul></ul><ul><ul><li>Nervousness </li></ul></ul><ul><ul><li>Tachycardia </li></ul></ul><ul><ul><li>Tremor </li></ul></ul><ul><ul><li>Hunger </li></ul></ul><ul><ul><li>Diaphoresis </li></ul></ul><ul><ul><li>Pallor </li></ul></ul><ul><ul><li>Paresthesias </li></ul></ul><ul><li>Neuroglycopenic </li></ul><ul><ul><li>Headache </li></ul></ul><ul><ul><li>Mental illness </li></ul></ul><ul><ul><li>Inability to concentrate </li></ul></ul><ul><ul><li>Slurred speech </li></ul></ul><ul><ul><li>Blurred vision </li></ul></ul><ul><ul><li>Confusion </li></ul></ul><ul><ul><li>Irrational behavior </li></ul></ul><ul><ul><li>Lethargy </li></ul></ul><ul><ul><li>LOC, coma, seizure </li></ul></ul>
  89. 90. Interventions <ul><li>Mild </li></ul><ul><ul><li>carbohydrate 10-15 gram </li></ul></ul><ul><li>Moderate </li></ul><ul><ul><li>20-30 gram of carbs </li></ul></ul><ul><ul><li>Glucagon, 1 mg SC or IM </li></ul></ul><ul><li>Severe </li></ul><ul><ul><li>50% dextrose 25 g IV </li></ul></ul><ul><ul><li>Glucagon 1 mg IM or IV </li></ul></ul>
  90. 91. Diabetes in Pregnancy <ul><li>Early pregnancy (<24 weeks) </li></ul><ul><ul><li>Rapid embryo growth </li></ul></ul><ul><ul><li>Decrease in maternal blood glucose </li></ul></ul><ul><ul><li>Episodes of hypoglycemia </li></ul></ul>
  91. 92. Diabetes in Pregnancy <ul><li>Late pregnancy (>24 weeks) </li></ul><ul><ul><li>Increased resistance to insulin effects </li></ul></ul><ul><ul><li>Increased blood glucose </li></ul></ul><ul><ul><li>Ketoacidosis </li></ul></ul>
  92. 93. Diabetes in Pregnancy <ul><li>Increased maternal risk for: </li></ul><ul><ul><li>Pregnancy-induced hypertension </li></ul></ul><ul><ul><li>Infections </li></ul></ul><ul><ul><ul><li>Vaginal </li></ul></ul></ul><ul><ul><ul><li>Urinary tract </li></ul></ul></ul>
  93. 94. Diabetes in Pregnancy <ul><li>Increased fetal risk for: </li></ul><ul><ul><li>High birth weight </li></ul></ul><ul><ul><li>Hypoglycemia </li></ul></ul><ul><ul><li>Liver dysfunction-hyperbilirubinemia </li></ul></ul><ul><ul><li>Hypocalcemia </li></ul></ul>
  94. 95. Acute Complications of Diabetes <ul><li>Compare </li></ul><ul><ul><li>DKA </li></ul></ul><ul><ul><li>HHNK </li></ul></ul><ul><ul><li>Hypoglycemia </li></ul></ul><ul><ul><li>see chart for comparison </li></ul></ul>
  95. 96. Other Complications <ul><li>Hypoglycemic Unawareness </li></ul><ul><li>Somogyi Phenomenon </li></ul><ul><li>Dawn Phenomenon </li></ul>
  96. 97. Chronic Complications <ul><li>Macrovascular Complications </li></ul><ul><li>Microvascular Complications </li></ul><ul><li>Neuropathic Complications </li></ul><ul><li>Mixed </li></ul>
  97. 98. Foot Infections with Diabetes <ul><li>Inspection </li></ul><ul><li>Footwear </li></ul><ul><li>Foot Care </li></ul>
  98. 99. Microvascular Complications <ul><li>Retinopathy </li></ul><ul><li>Nephropathy </li></ul>
  99. 100. Visual Complications of Diabetes <ul><li>Education of client </li></ul><ul><ul><li>Diabetic retinopathy can lead to blindness </li></ul></ul><ul><ul><ul><li>Check blood sugar </li></ul></ul></ul><ul><ul><ul><li>Check blood pressure </li></ul></ul></ul><ul><ul><ul><li>Regular eye exam with ophthalmologist </li></ul></ul></ul><ul><ul><ul><li>Laser photocoagulation therapy </li></ul></ul></ul>
  100. 102. THANK YOU !
  101. 103. <ul><li>Long-term control of blood glucose reduces the rate and severity of complications </li></ul><ul><li>But even short-term glycemic control in hospitalized patients can significantly lower morbidity and mortality in many areas, from nosocomial infection to postoperative course </li></ul>
  102. 104. <ul><li>The results of traditional approaches to controlling blood glucose in hospitalized patients have been disappointing owing to a variety of factors: </li></ul><ul><ul><li>use of oral agents that are difficult or dangerous to use in inpatients </li></ul></ul><ul><ul><li>older insulin preparations with unphysiological modes of action </li></ul></ul><ul><ul><li>and even provider reluctance to accept glycemic control as an essential element of the care of the diabetic hospitalized patient </li></ul></ul>
  103. 105. <ul><li>The end point of each of the different etiologies is hyperglycaemia </li></ul><ul><li>The adverse effects of hyperglycaemia are both acute and chronic </li></ul>
  104. 106. <ul><li>These need to be treated aggressively as the mortality of ketoacidosis is still estimated as up to 15% </li></ul><ul><li>Hyperosmolar non-ketotic hyperglycaemic coma may carry an even higher mortality. </li></ul><ul><li>This is probably because this is an older group with a higher incidence of co-existing disease </li></ul>