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Anesthetic implications of diabetes mellitus

Anesthetic implications of diabetes mellitus. Moderator Dr Dara Negi Dr Avinash Goyal. Introduction. the prevalence of diabetes mellitus (DM) is rapidly increasing throughout the world

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Anesthetic implications of diabetes mellitus

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  1. Anesthetic implications of diabetes mellitus Moderator Dr DaraNegi Dr AvinashGoyal

  2. Introduction the prevalence of diabetes mellitus (DM) is rapidly increasing throughout the world physicians will be confronted with an increasing population of diabetic patients undergoing anesthesia and surgery A significant number with type 2 DM are unaware that they are diabetic until the time of surgery. Diabetics have higher morbidity and mortality as surgical patients. End-organ effects of diabetes are more important to periop outcome Tighter the control of glucose desired, more frequently glucose levels to be measured

  3. PHYSIOLOGICAL IMPACT • 6th leading cause of death by disease • Decreases life expectancy of middle-aged people by 5-10 years • 2-4 x greater risk of death d/t heart disease • Leading cause of blindness in 25-74 year olds • Leading cause of non-traumatic amputations • Responsible for 25-30% of all new dialysis patients

  4. Diabetes mellitus results from an inadequate supply of insulin and/or an inadequate tissue response to insulin, yielding increased circulating glucose levels with eventual microvascular and macrovascular complications.

  5. DIAGNOSIS As per American Diabetes association (ADA) A normal fasting plasma glucose is 70 to 100 mg/dL. A random plasma glucose concentration of 200 mg/dL or higher, with classical signs and symptoms (polyuria,polydyspia,unexplained weight loss) or A fasting (no calorie intake >8hrs)plasma glucose concentration of 126 mg/dL or higher or An abnormal oral glucose tolerance test (OGTT), in which the glucose concentration is 200 mg/dL or higher 2 hours after a standard carbohydrate load (75 gm of glucose).

  6. Glucose • whole blood values are 10-15% lower than plasma/serum • Venous blood values are 10% lower than capillary/arterial. • Venous blood - loss of 0.33 mmol/L per hour • There is no decrease within 24 h in the presence of sodium fluoride

  7. Impaired Fasting Glucose • Any fasting glucose between 101 and 125 mg/dL • Increased risk for DM • Must educate regarding risks and need for lifestyle modifications

  8. IMPAIRED GTT • Defined as a plasma blood glucose of >/= to 140 but < 200 after a 2 hour 75 gram glucose tolerance test • 8-10% of population have this problem with a 25 % risk of developing DM 2 • Compounding risk factors effect risk of developing Type 2 DM • Age • Activity • Comorbidities • Weight • Increased risk for macrovascular diseases • Must educate regarding risks and need for lifestyle modifications

  9. HEMOGLOBIN A1c • provides a valuable assessment of long-term glycemic control • Erythrocyte hemoglobin is nonenzymaticallyglycosylated by glucose • HbA1c is stable glycosylatedhemoglobin • Its percentage concentration indicates average plasma glucose • concentration during the preceding 60 to 90 days. • Performed 2 times a year. • The normal range for Hb A1c is 4% to 6%. • Increased risk of microvascular and macrovascular disease begins at a Hb A1c of 6.5%. • Lowering HbA1C Reduces Risk of Complications

  10. Glucose physiology • Glucose is a crucial fuel source • insulin facilitates glucose movement into cells • Red blood cells, healing wounds, the brain, and the adrenal medulla require glucose approximately @ 2 mg/kg/min. • Daily requirement of glucose for 70 Kg man is 200gm/day(90-100g stored as glycogen)

  11. Normal glucose homeostasis is tightly regulated by three interrelated processes • glucose production in the liver, (2) glucose uptake and utilization by peripheral tissues, chiefly skeletal muscle, (3) actions of insulin and counter-regulatory hormones (e.g., glucagon).

  12. Metabolic problem • Diabetes is generalised catabolic state • Lipids are mobilized with release of fatty acids • Ketogenesis leads to acidosis & loss of cellular potassium • Gulconeogenesis & glycogenolysis ,with decreased peripheral glucose utilization causes hyperglycemia • Glycosuria causes osmotic polyuria & dehydration • Plasma hyperosmolarity ,acidosis,hyperkalemia results leading to coma & death

  13. GLUCOTOXICITY: high levels of glucose causes • nonenzymaticglycosylation reactions that lead to the formation of abnormal proteins which weaken endothelial junctions and decrease elastance, which is responsible for the stiff joint syndrome (and difficult intubation secondary to fixation of the atlanto-occipital joint), as well as decrease wound-healing tensile strength. •   increase macroglobulin production by the liver (which would increase blood viscosity) and promote intracellular swelling by favoring the production of nondiffusible, large molecules (such as sorbitol). • Glycemia also disrupts autoregulation. Glucose-induced vasodilation prevents target organs from protecting against increases in systemic BP.

  14. DM TYPE I • Constitutes 5-10% of DM diagnosed • Mostly appears in children and young adults • caused by a T cell–mediated autoimmune destruction of beta cells of the pancreas. • At least 80% to 90% of beta-cell function must be lost before hyperglycemia occurs • A long preclinical period (9–13 years) • presentation of clinical disease is often sudden and severe , Patients demonstrate hyperglycemia over several days to weeks • associated with fatigue, weight loss, polyuria, polydipsia, blurring of vision, and signs of intravascular volume depletion • The diagnosis is based on • : a random blood glucose greater than 200 mg/dL • hemoglobin (Hb) A1c level greater than 7.0%. • ketoacidosis indicates severe insulin deficiency and unrestrained lipolysis. • Beta-cell destruction is complete within 3 years of diagnosis , with the process being slower in adults. • TREATMENT-INSULINt

  15. DM TYPE II • Most common form of diabetes • Involves about 90-95% of people with DM • most type 2 diabetics have had the disease for approximately 4 to 7 years before it is diagnosed • Associated with: • older age • obesity • family history of DM • prior history of gestational diabetes • physical inactivity • Ethnicity • Patient with type II DM usually makes enough insulin but the body cannot use it effectively => insulin resistance • Gradually insulin production decreases over the following years • Symptoms are similar to type I but develop more gradually • TREATMENT- diet control ( wt loss),exercise & medications (OHGs)

  16. Gestational diabetes • Hyperglycemia first diagnosed during pregnancy • Occurs in 2-5% of pregnancies • Occurs due to placental hormone changes that effect insulin function (greater resistance) • Screening usually occurs during the 24th-28th week in high risk patients • Criteria for diagnosis is different than for Type 1 and Type 2 • Dietary changes are initial treatment and insulin is the only BG lowering agent used • Better maternal glycemic control lowers the incidence of neonatal hypoglycemia and hyper bilirubinemia • Postpartum BG levels usually return to normal • Women with a history of gestational diabetes have a 20-50% chance of getting type II DM within 5-10 years

  17. SECONDARY DM • DM occurs as a result of another problem (primary) • Medications • Thiazides • Diuretics • Beta blockers • Steroids • Treatment of the primary cause may resolve the DM but lifestyle modifications and medications may be needed as well

  18. DRUG THERAPY IN DM • Oral Diabetic Medications • Sulfonylureas-gliclazide,tolbutamide increases insulin release longer duration of action • Biguanides-(Metformin) potentiates insulin causes lactic acidoses in dehydrated pts • Alpha-Glucosidase (acarbose) Inhibitors-decrease absorption of glucose • NonsulfonylureaSecretagogues • Meglitinide • D-phenylalanine derivatives • Thiazolidinediones (TZDs)-rosiglitazone

  19. Insulins • Short acting - Soluble / Neutral insulin Insulin aspart Insulin lispro • Intermediate acting - Isophane • Long acting - Insulin Zinc suspension new insulin analogue - Glargine Detemir • Biphasic- mixture of short and intermediate Biphasic lispro Biphasic Isophane

  20. Types of insulin

  21. Complications of DM • ACUTE • Metabolic • Diabetic ketoacidosis(DKA) • Hyperosmolar Hyperglycemic Nonketotic Syndrome(HHNS) • Hypoglycemia • Infections • CHRONIC • Microvascular • Retinopathy • Nephropathy • Macrovascular • CAD • CVD • PVD • Neuropathies • Diabetic Foot Disorders • Psychosocial concerns

  22. DIABETIC KETOACIDOSIS (DKA) Signs and symptoms • Hyperglycemia (>300mg/dl) • Elevated serum ketones • Acidosis as evidenced by pH of 6.8-7.3 • HCO3 < 18 • Osmolarity <320 • Dehydration • Electrolyte depletion • GI distress (abdominal pain, N/V) • Respiratory distress (Kussmaul’s respirations and acetone breath odor)

  23. TREATMENT OF DKA Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. • Correction of fluid loss with intravenous fluids • Correction of hyperglycemia with insulin • Correction of electrolyte disturbances, particularly potassium loss • Correction of acid-base balance • Treatment of concurrent infection, if present

  24. Correction of Fluid Loss • Rehydration alone reduces plasma glucose by 30-50% • Initial correction of fluid loss is either by isotonic sodium chloride solution or by lactated Ringer solution. The recommended schedule for restoring fluids is as follows: • Administer 1-3 L during the first hour.(15-20ml/kg) • Administer 1 L during the second hour. • Administer 1 L during the following 2 hours • Administer 1 L every 4 hours, depending on the degree of dehydration and central venous pressure readings • When blood sugar decreases to less than 250 mg/dL, isotonic sodium chloride solution is replaced with 5-10% dextrose with half isotonic sodium chloride solution.

  25. Insulin therapy • Loading dose of 0.1U/kg i.v. of regular insulin • Followed by infusion of 0.1U/kg per hour • Average decline of plasma glucose should be 75-100ml/hr with target values around 250ml/dl

  26. Electrolyte Correction • If the potassium level > 6 mEq/L, do not administer potassium supplement. • If the potassium level is 4.5-6 mEq/L, administer 10 mEq/h of potassium chloride. • If the potassium level is 3-4.5 mEq/L, administer 20 mEq/h of potassium chloride. • Monitor serum potassium levels hourly,

  27. Correction of Acid-Base Balance • Bicarbonate typically is not replaced as acidosis will improve with the other treatments alone. • Administration of bicarbonate has been correlated with cerebral edema in children. • Sodium bicarbonate is infused if decompensated acidosis starts to threaten the patient's life(pH <7.1) • If sodium bicarbonate is indicated, 100-150 mL of 1.4% concentration is infused initially. This may be repeated every half hour if necessary. • Treatment of Concurrent Infection

  28. Hyperosmolar Hyperglycemic Nonketotic Syndrome(HHNS) • Four Clinical Features • Hyperglycemia (> 600-2000) • Mild or no ketosis • Hyperosmolality of plasma or serum (>340) • Profound dehydration • 10-20% mortality rate with HHNS • Risk factors include • Elderly with Type 2 • Undiagnosed DM • Prolonged hyperglycemia • Signs and Symptoms • Hypotension • Dehydration • Tachycardia • Decreased mentation • Neurologic abnormalities (focal)

  29. Treatment • If the plasma osmolarity > 320 mOsm/L, large volumes (1000–1500 mL/hr) of 0.45% normal saline should be administered until the osmolarity is less than 320 mOsm/L,followed by 0.9% normal saline Insulin infusion @ 0.1U/kg hr Electrolyte disturbances are less severe compared to DKA

  30. hypoglycemia • plasma glucose level less than 50 mg/dL. • May occur in all types of DM and is usually related to illness • Causes • Excessive exogenous insulin or oral diabetes medications that increase insulin production • Excessive alcohol consumption especially w/o adequate food intake • Impaired hepatic or renal function • Too little food • Excessive exercise • Signs and symptoms adrenergic (sweating, tachycardia,palpitations, restlessness, pallor) and neuroglycopenic (fatigue,confusion, headache, somnolence, convulsions,coma).

  31. TREATMENT OF HYPOGLYCEMIA • Mild (40-60 gm/dl) • Ingestion of 15 grams of Carbohydrate • Monitor BG levels and treat until euglycemia • Educate to prevent • Moderate (20-40 gm/dl) • Ingestion of 15-30 grams of CHO and follow with a meal or snack containing protein • Monitor BG levels and treat until euglycemia • Educate to prevent • Severe (<20 gm/dl) • Ingestion not possible-must use IV glucose 0.5 g/kg IV or IM glucagon 0.5 to 1.0 mg preferably. • May use glucose gel, honey, syrup, or jelly inside cheek • Monitor BG levels and treat until euglycemia • Educate to prevent • Each ML of 50% glucose will raise BG by 2 mg/dl

  32. WOUND HEALING & INFECTIONS Wound healing is impaired in diabetic pts Infections are the common cause of diabetic complications • Alterations in leukocyte function- • ↓ chemostasis • Impaired phagocytic activity • Reduced intracellular killing • Commonly seen infections • Cutaneous-furunculosis and carbuncles • Vulvovaginits • Cellulitis • UTI • Ear • Must be treated aggressively

  33. MICROVASCULAR COMPLICATIONS • Microangiopathies affecting the capillaries and arterioles of tissues • Retina (retinopathy) • Renal glomeruli (nephropathy) • RETINOPTHY • Development and progression largely depend on the duration and severity of hyperglycemia • Early detection and treatment can be beneficial in visual restoration • Uncontrolled HTN is an aggravating factor • 3 categories • Nonproliferative • Preproliferative • proliferative

  34. NEPHROPATHY • 20-40% chance of developing with a diagnosis of DM • Earlier occurrence in Type 2 than Type 1 DM • Glomerulosclerosis with glomerular basement membrane thickening • 39-54% decrease in development with tight BGcontrol (DCCT) • Signs and symptoms • Microalbuminuria/proteinuria • Elevated creatinine clearance • Aggrevating conditions • HTN • Neurogenic bladder/UTI/Nephrotoxic drugs • Treatment • Improving BG control • HTN management (ACE inhibitors) • Protein restriction • Dialysis/kidney transplant • Educate to prevent

  35. MACROVASCULAR COMPLICATIONS • Responsible for 80% of deaths in people with DM • Major vessels affected • Coronary arteries • Cerebral arteries • Peripheral arteries • CORONARY • MI risk is 2x> in men and 3x> in women with DM • Treatment-Aimed at reducing modifiable risk factors • Smoking cessation • BG, HTN, and lipid control • Medications may include ACE or ARBs, statin drugs, and ASA • Exercise (focus on wt reduction) • CEREBRAL • 2x> risk of CVD in patients with DM • PERIPHERAL • 2-3x> risk in patients with DM • Signs and symptoms include IC, diminished peripheral pulses, lower extremity hair loss, and nocturnal rest pain • Major factor in the development of gangrene and amputations in patients with DM • Treatment • Aimed at modifiable risk factors as listed with CAD • Medication • Rest during periods of exertion

  36. Peripheral neuropathy • 50% of diabetics develop peripheral neuropathy after 25 years • Distal symmetrical diffuse sensorimotorpolyneuropathy is most common(stocking glove neuropathy) • Foot ulcers develop due to loss of cutaneous sensitivity to pain and temp and impaired perfusion • Treatment includes optimal glucose control ,NSAIDS,Antidepressants,anticonvulsants for pain relief

  37. Diabetic Autonomic Neuropathy • affect any part of the autonomic nervous system. • Autonomic disturbances can be subclinical or clinical • Subclinical DAN can occur within a year or two after diagnosis • Cardiovascular autonomic neuropathy is a common type of DAN • A resting tachycardia and a loss of heart rate variability (HRV)(<10 beats per min)during deep breathing are early signs. • in the advance stages, severe orthostatic hypotension (>30 mm Hg with standing) is present. • Impaired respiratory reflexes and impaired ventilatory responses to hypoxia and hypercapnia are also present

  38. Gastrointestinal effects of DAN • Affects 25% of diabetics • impair gastric secretion and gastric motility, causing gastroparesisdiabeticorum • nausea, vomiting, early satiety, bloating, and epigastric pain. • In DAN, the counterregulatory hormone responses to hypoglycemia are impaired and the warning signs eliminated, creating a dangerous situation of hypoglycemia unawareness.

  39. Diabetes and accelerated physiologic ageing(“RealAge”)(‘X’ yrs for each choronologic yr of disease)Diabetes cause accelerated aging Thus, the risks involved with diabetes are similar to those for someone much older, someone who has a much higher physiologic age (or “RealAge”).

  40. Acute hyperglycemia causes • dehydration, • impaired wound healing, • an increased rate of infection, • worsening central nervous system/spinal cord injury with ischemia, • hyperviscosity with thrombogenesis

  41. Preop evaluation • History & general physical exam • MEASURE BLOOD PRESSURE AND PULSE RATE- BOTH WHEN THE PATIENT IS LYING DOWN AND STANDING • ASSESS THE PATIENT'S MUSCLE STRENGTH, DEEP TENDON REFLEXES, AND SENSE OF TOUCH. • HBA1c levels • Pulmonary,Cardiovascular & renal assessment • CXR-cardiac enlargement,pleural effusion, pulmonary vascular congestion • ECG • TM & C-spine mobility • No insulin ,no glucose for short procedures

  42. Pre-op evaluation Autonomic Neuropathy • typical symptoms and signs of postural hypotension, gastroparesis, gustatory sweating, and nocturnal diarrhoea. • It is worth assessing all diabetic patients for autonomic neuropathy. • The easiest way is to assess heart rate variability. The normal heart rate should increase by over 15 beats/minute in response to deep breathing. Neuropathy is likely is there is less than 10 beats/minute increase

  43. Peripheral Neuropathy • The commonest type of peripheral neuropathy is the “glove and stocking” type. • However diabetics are also prone to mononeuritis multiplex and some particularly painful sensory neuropathies. • Poor patient positioning is likely to result in pressure sores that are often slow to heal given poor peripheral blood flow. • Documentation of existing neuropathy is prudent, especially if considering a regional technique.

  44. Cardiovascular • Diabetics are more prone to ischaemic heart disease (IHD), hypertension, peripheral vascular disease, cerebrovascular disease, cardiomyopathy and perioperative myocardial infarction. • Ischaemia may be “silent” as a result of neuropathy. Routine ECG should be performed and appropriate stress testing if in doubt. • Autonomic neuropathy can result in sudden tachycardia, bradycardia, postural hypotension and profound hypotension after central neuraxial blockade

  45. Respiratory • Diabetics, especially the obese and smokers are more prone to respiratory infections and also have abnormal spirometry. • Chest physiotherapy, humidified oxygen and bronchodilators should be considered

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