Anesthetic Management Of Pediatric Diabetes mellitus<br />Prof. Dr. AzzaEzzat<br />Professor of Anesthesiology <br />Cairo University<br />
Dealing with diabetic child is a challenge , not only to the anesthiologist but also to endocrinologist .<br />Why?<br />It is difficult to control their meals <br />It is also difficult to put them on diet regimens<br />Limited management options <br />Frequent injection (fear of repeated insulin injection )<br />
Our aim<br />Is to do safe perioperative management <br />Providing balanced glycemic control<br />Avoiding hypoglycemia with its serious brain insult in this age group.<br />Also preventing excessive hyperglycemia with it’s dangerous sequel.<br />
Pancreas<br /><ul><li>The pancreas is a dual function gland
Pancreatic juice</li></ul> both are secreted into the <br /> small intestine directly <br />
Regulation of insulin secretion<br />Insulin is secreted into the portal venous system in the basal state at rate of approximately 1 u/h .<br />Food intake results in a prompt five to ten fold increase in the rate of insulin secretion <br />Insulin is not secreted when the blood glucose level <50 mg /dl <br />Max. stimulation of insulin release when blood glucose level >300 mg/dl <br />
Role of insulin <br />It facilitates transport of glucose across cell membranes and enhances phosphorylation of glucose within cells<br />It promotes the use of CHO for energy conservation while depressing the use of fat and amino acids<br /><ul><li>Increases glucose and K entry into the cells</li></ul>Excess glucose is stored in :<br /> -The liver as glycogen <br /> -Adipose tissue as fat <br /> -Skeletal muscle as protein and glycogen <br />
Sequels of insulin deficiency<br /><ul><li>Glycogenolysis
Protein catabolism</li></ul>So insulin stimulates ANABOLISM and prevents CATABOLISM <br />
Diabetes Mellitus<br />Prevalence: 0.7/1000 this is according to 2007 records at the Cairo university pediatric hospital<br />Follow-up: 6000 children<br /><ul><li>Risk factors include:
environmental e.g. viral infection
genetic predisposition</li></li></ul><li>Diabetes Mellitus<br />Decreased or diminished effectiveness of insulin <br />Characterized by impairment of carbohydrate metabolism<br />Resulting in hyperglycemia and glycosuria<br />Plasma 140 mg / dl <br />Blood > 126 mg / dl <br />FBS<br />Plasma contains 12% more sugar<br />
Classification of diabetes <br />
Pathophysiology<br />Insulin deficiency causes physiologic and metabolic changes in the body<br />Glucose from dietary sources cannot be utilized by the cells<br />Renal tubules have difficulty reabsorbing the glucose<br />
Pathophysiology<br /><ul><li>If the blood glucose level exceeds the renal threshold for glucose osmotic diuresis ensues.
Renal threshold: when serum glucose levels approach 200mg/dl the renal tubules have difficulty re-absorbing the glucose
Hyperglycemia impairs leukocyte function.</li></li></ul><li>Clinical Manifestations<br />Elevated blood glucose leads to osmotic diuresis. (polyuria and thirst)<br />Protein and fat breakdown lead to weight loss.<br />Accumulation of ketones causes a drop in pH. (metabolic acidosis) and spilling of ketones in the urine<br />
Presenting Symptoms<br /><ul><li>Hyperglycemia / glucose in blood stream
Glucosuria / sugar in urine
Polyuria / increased urine output
Electrolyte imbalance from dehydration
Polydipsia / attempt to relieve dehydration
Polyphagia / attempt to compensate for lost calories</li></li></ul><li>Diagnostic Tests<br />Blood glucose levels greater than 200 mg/dl<br />Urine sample reveals glucosuria and possible ketonuria<br />Glucose tolerance test would reveal low insulin levels in the face of elevated glucose levels<br />
Goals of Management<br />Short term goals:<br />Prevent the development of ketosis.<br />Prevent electrolyte abnormalities and volume depletion secondary to osmotic diuresis.<br />Prevent impairment of leukocyte function <br />Prevent impairment of wound healing <br />Long term goal: prevention of microcirculatory and neuropathic changes<br />
Blood Glucose Levels<br />Target levels<br />Toddler and preschool: 100 to 180 mg/dl<br />School-age: 90 to 180 mg/dl<br />Adolescents (13 to 19 years): 90 to 130 mg/dl<br />
Common types of DM in pediatrics<br />Type 1 DM which is caused by pancreatic β cell destruction usually immune mediated. It results in absolute insulin deficiency. Incidence (11.7- 17.8/ 100000).<br />Type 2 DM results from a combination from insulin resistance and relative deficiency of insulin.* <br /> *Diabetes Care 2004 <br />
Management Options for DM in Pediatrics<br /><ul><li>Insulin regimens</li></ul> Insulin regimens incorporate a combination of intermediate and long acting insulin with short or rapid insulin (2-3 injections/day)<br /> Insulin Pump (SC)<br /> Continuous administration of rapid <br /> acting insulin at a basal rate <br /> and supplemented with additional <br /> doses before meal or snacks.<br />
An easy to handle insulin pump<br />
Insulin Preparations classified according to pharmacodynamic profiles<br />
Short Acting Insulin<br /><ul><li> Short acting (Soluble, Regular) insulin is used as an essential component of most daily replacement regimens.</li></ul>- In combination with intermediate acting insulin - As premeal bolus injections 20-30 minutes before meals.<br />- It is the only insulin suitable for IV therapy.<br />
Rationale for insulin Glargine<br />Insulin glargine was designed to provide a constant basal insulin concentration to control basal metabolism with one injection daily<br />Insulin Glargine is indicated for the treatment of adult and pediatric patients (over the age of 6 years) with type I diabetes.<br />
Summary of types of insulin<br />Rapid acting = ultra short (neonates & infants) with meal (lactation)<br />Short acting = regular insulin (all ages)<br />Intermediate at basal rate (children & infants)<br />Long acting (pre puberty i.e. 10 years)<br />Galargine (not less than 6 years if used pre puberty)<br />
Oral Antihyperglycemics<br />Metformine is the only drug approved in pediatric population.<br />Action:<br /> - It decreases hepatic glucose production.<br /> - It increases insulin sensitivity in peripheral tissues. <br />
Metabolic Response for Surgery and Anesthesia<br /><ul><li>Suppression of insulin secretion.
Increased production of counter regulatory hormones ( Cortisol, Catecholamines, GH, Glucagon)
NPO (starvation) has catabolic effect leading to lipolysis and glycogenolysis.
Transient phase of insulin resistance after surgery. *</li></ul> *Angelini G, 2001<br />
Preoperative Assessment<br />Blood Glucose<br />Metabolic Control<br />Electrolyte balance<br />Glycosylated Hb<br /> ↓ 5 years 7% to 9%<br /> 5-13 years 6% to 8.5%<br /> ↑ 13 years 6% to 8%<br />
On the day of surgery Short procedure<br />Withhold morning dose<br />Glucose-free solution<br />When postoperative oral intake is established 40 – 60 % of usual daily dose is administered <br />
On the day of surgeryLong ProcedureIf Blood Glucose 100 – 200 mg/dl <br />Hold rapid or short acting insulin.<br />Administration 50% the intermediate or long acting insulin.<br />Omit breakfast<br />Patient scheduled first case (Avoid starvation).<br />Rhodes et al 2005<br />
Insulin Infusion<br /> - Add soluble insulin 50 units to 50 ml NS 0.9%.<br /> - Start infusion at: <br />0.025 ml/kg/h if blood glucose is < 6-7 mmol/l<br /> 0.05 ml/kg/h if blood glucose is 8-12 mmol/l<br /> 0.075 ml/kg/h if blood glucose is 5-10 mmol/l<br /> 0.1 U/kg/h if blood glucose is > 15 mmol/l<br /> - Aim to maintain BG between 5-10 mmol/l .<br /> - BG must be measured at least hourly when the patient is on IV inf.<br /> - Do not stop the insulin infusion if BG < 5-6 mmol/l (90 mg/dl) as this will cause rebound hyperglycemia. Reduce the rate of infusion.<br /> - The insulin infusion may be stopped temporarily if BG < 4mmol/l (55 mg/dl) but only for 10-15 min.<br />Bett et al 2009 <br />
On the day of surgeryLong ProcedureIf Blood Glucose > 250 mg/dl <br />On the morning of surgery: <br />No rapid or short-acting insulin is given unless blood glucose is > 250 mg/dl<br />>250 mg/dl give a dose of rapid-acting insulin using “correction factor”<br />Correction factor: The decrease in blood glucose level expected after administering 1 unit of rapid acting insulin<br />
How to calculate corrective dose?<br />Using the rule of 1500 for regular insulin<br />Example:<br />The total daily dose of a child is 30 U<br />So the correction factor = 1500/30 = 50<br />i.e. each unit of insulin will decrease his blood glucose level by 50 mg/dl<br />If this child’s blood glucose level = 300 mg/dl and his target glucose level = 150 mg/dl<br /> his corrective dose = 300 – 150/50 = 3 U<br />OR<br />0.1 u/kg SC of rapid acting insulin<br />
Anesthetic management<br /><ul><li>Scheduling the diabetic child as the first case to shorten the fasting hours (NPO like non diabetic)
Use of premedication
No premedication: to monitor signs and symptoms of hypoglycemia
Premedication: Anxiety may increase blood glucose level</li></ul>The Aim is to keep blood glucose 100 – 200 mg/dl<br />Keep Them Sweet<br />
Metformin withhold 24 hrs preoperative<br />Sulfonylurea withhold on morning of surgery<br />Preoperative for child on Oral Hypoglycemics<br />
Intraoperative<br />Keep blood glucose 100-200 mg/dl.<br />Potassuim: assessment of level of electrolyte especially in lengthy procedures.<br />Fluid maintenance 1500 ml/m2/day.<br />Iv insulin<br /><12 years: 1 u/5g glucose<br />>12 years: 1 u/3g glucose<br />
Postoperative Management<br /><ul><li>Once the child resumes oral intake restart his insulin or oral hypoglycemic regimen.
Insulin dosing for previously non diabetic children
0.6 – 0.8 U/kg/day (prepuberty)
1 – 1.5 U/kg/day (Adolscence)</li></li></ul><li>Hypoglycemia<br />Blood glucose level<br /> < 60 mg / dl ( children )<br /> < 40 mg / dl (neonates ) <br />Diabetic patients can not combat hypoglycemia by secreting glucagon and adrenaline<br />
Administer 2 mL/kg of D10%W followed by a continuous infusion of 6-8 mg/kg/min to maintain blood glucose level 70-120 mg/dl
0.5-1 g/kg, which is equal to 2-4 ml/Kg of D25% or 5-10 ml/Kg of D10% or 10-20 ml/Kg of D5%
If hypoglycemia persists, you may increase glucose infusion to 8-15 mg/kg/min.</li></li></ul><li>Diabetic Ketoacidosis<br /><ul><li>Definition : Diabetic ketoacidosis (DKA) is a complex metabolic state of hyperglycemia, ketosis, and acidosis
Infection is the most frequent cause of diabetic ketoacidosis, particularly in patients with known diabetes
Missed insulin doses
Pathophysiology :</li></ul>Hyperglycemia Osmotic diuresis loss of free water and electrolytes Hypovolemia tissue hypoperfusion and lactic acidosis<br />The ketoacids (acetoacetate, beta-hydroxybutyrate, acetone) are products of proteolysis and lipolysisKETOACIDOSIS<br />Potassium is the most important electrolyte in patients with severe diabetic ketoacidosis ( Hyperkalemia or Hypokalemia)<br />
Management<br /><ul><li>The goal of the first hour of treatment
confirmation of diabetic ketoacidosis by laboratory studies
Management of urgent airway, breathing, and circulation
Fluid therapy :
Isotonic sodium chloride solution bolus, 20 mL/kg intravenously over an hour or less then gradual replacement over the succeeding hours
Add 5% dextrose to intravenous fluids, if the child remains in ketoacidosis and serum glucose level approaches 250-300 mg/dL
The goals of the second and succeeding hours :</li></ul>slow correction of hyperglycemia (with glucose level falling at a rate <100 mg/dL/h), metabolic acidosis, and ketosis, in addition to continued volume replenishment<br /><ul><li>Insulin :
Do not give insulin until severe hypokalemia is corrected
Then give 0.1 U/kg regular insulin intravenous bolus; follow with insulin 0.1 U/kg/h intravenously by constant infusion</li></li></ul><li><ul><li>Do not discontinue the insulin drip, as the child remains in ketoacidosis for some time and insulin is critical in eliminating ketoacidosis
Initiate insulin therapy after beginning fluid replacement and serum potassium correction
Once the child has been resuscitated, potassium should be commenced immediately with rehydration fluid unless anuria is suspected
Potassium is mainly an intracellular ion, and there is always massive depletion of total body potassium although initial plasma levels may be low, normal or even high
Levels in the blood will fall once insulin is commenced
If serum potassium level is greater than 5.5 mmol per litre, do not add additional potassium to intravenous fluids
The final goal is to obtain a serum glucose concentration within the reference range (serum glucose level, 100-150 mg/dL), to obtain neutral blood pH (pH =7.4; serum bicarbonate = 15-18 mEq/dL), and to eliminate serum ketones.
Identification and treatment of the precipitant event, antibiotic for infection
Hourly monitoring of serum markers of diabetic ketoacidosis</li></li></ul><li>Remember<br /><ul><li>Assess for other associated endocrine or congenital disease.
Fasting diabetic child should be scheduled first case.
Elective cases should be euglycemic.
Avoid drugs that increase blood glucose e.g. ketamine and pancronium.
Target blood glucose level is 100-200 mg/dl.</li></li></ul><li>Remember<br /><ul><li>Insulin should be infused through a separate line.
The decrease in blood glucose level should be at a rate not more than 50-100 mg/dl/hr.
Glucose 25% is not used in pediatrics (vascular injury).
Assess blood glucose level every 1-1.5 hr.
0.1 g/kg dextrose will raise blood glucose level by about 30 mg/dl.</li></li></ul><li>Remember<br />Adequate planes of anesthesia and analgesia is necessary to avoid hyperglycemia secondary to stress response or lack of analgesia. <br />
Thank You<br />
Pancreas<br /><ul><li>b cells of Islets of Langerhans secret 50 units of insulin /day
Secretion determined by blood glucose level
Increases glucose and K entry into the cells
Increased synthesis of Glycogen, Protein and fatty acid synthesis </li></li></ul><li> Effects of insulin on liver<br />Anabolic <br /><ul><li>Promotes glycogenesis