Anesthesia for Patient with Diabetis Mellitus

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Anesthesia for patient with diabetis mellitus

Classification of diabetes mellitus

· Type 1 diabetis mellitus, formerly known as juvenile or IDDM

· Type 2 diabetis mellitus , formerly known as NIDDM

· Type 3 diabetis mellitus

· Type 4 diabetis mellitus or gestational diabetis mellitus

Physiology

· Adults normally secrete approximately 50 U of insulin each day from the cells of the islets of Langerhans in the pancreas.

· The rate of insulin secretion is primarily determined by the plasma glucose level.

Endocrinologic Effects of Insulin.1

Effects on liver    Anabolic     Promotes glycogenesis     Increases synthesis of triglycerides, cholesterol, and VLDL2       Increases protein synthesis     Promotes glycolysis   Anticatabolic     Inhibits glycogenolysis     Inhibits ketogenesis     Inhibits gluconeogenesis Effects on muscle    Promotes protein synthesis     Increases amino acid transport     Stimulates ribosomal protein synthesis   Promotes glycogen synthesis     Increases glucose transport     Enhances activity of glycogen synthetase     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

Clinical Manifestations

Overview

· Diabetes mellitus is characterized by impairment of carbohydrate metabolism caused by an absolute or relative deficiency of insulin or insulin responsiveness, which leads to hyperglycemia and glycosuria.

Diagnosis

· elevated fasting plasma glucose (> 140 mg/dL) or blood glucose (126 mg/dL).

Complications

CVS

· hypertension,

· coronary artery disease,

· myocardial infarction,

· congestive heart failure,

· diastolic dysfunction,

CNS

· peripheral and cerebral vascular disease,

· peripheral and autonomic neuropathies,

Renal

· renal failure.

Metabolic

· three life-threatening acute complications:

· DKA,

· hyperosmolar nonketotic coma

· hypoglycemia.

Diagnosis and Classification of Diabetes Mellitus.

Diagnosis (based on blood glucose level)    Fasting 126 mg/dL (7.0 mmol/L)   Glucose tolerance test 200 mg/dL (11.1 mmol/L) Classification    Type I Absolute insulin deficiency secondary to immune-mediated or idiopathic   Type II Adult onset secondary to resistance/relative deficiency   Type III Specific types of diabetes mellitus secondary to genetic defects   Type IV Gestational

Pathophysiology

· Decreased insulin activity allows the catabolism of free fatty acids into ketone bodies (acetoacetate and -hydroxybutyrate),

· Accumulation of these organic acids results in an anion-gap metabolic acidosis—DKA.

Diabetic ketoacidosis

· DKA can easily be distinguished from lactic acidosis, with which it can coexist; lactic acidosis is identified by elevated plasma lactate (> 6 mmol/L) and the absence of urine and plasma ketones (although they can occur concurrently and starvation ketosis may occur with lactic acidosis).

Alcoholic ketoacidosis

· Alcoholic ketoacidosis can be differentiated by a history of recent heavy alcohol consumption (binge drinking) in a nondiabetic patient with a low or slightly elevated blood glucose level.

· Such patients may also have a disproportionate increase in -hydroxybutyrate compared with acetoacetate.

Causes

· Infection is the most common cause of DKA, which in some patients, particularly adolescents, is the first manifestation of type I diabetes mellitus.

Presentation

· tachypnea (attempting to compensate for the metabolic acidosis),

· abdominal pain mimicking an acute abdomen, nausea and vomiting, and changes in sensorium.

· The treatment of DKA depends on first correcting the often substantial hypovolemia, the hyperglycemia, and the total body potassium deficit, with a continuous infusion of isotonic fluids and potassium, and an insulin infusion.

Goal of treatment

· The goal for decreasing blood glucose in ketoacidosis should be 75–100 mg/dL/h or 10%/h.

· Therapy can be begun with an intravenous infusion of 0.1 U/kg/h or the blood glucose value minus 60 times 0.1 U/h.

· These patients are often quite resistant to insulin therapy, and the rate may need to be increased if glucose levels do not decrease.

· As glucose moves intracellularly, so does potassium.

· Although this can quickly lead to a critical level of hypokalemia if not corrected, overaggressive replacement can cause an equally life-threatening hyperkalemia.

· Potassium, blood glucose, and serum ketones should be monitored no less often than every 2 h and preferably hourly.

Management

Dehydration

· Several liters of normal saline (1–2 L the first hour, followed by 200–500 mL/h) is typically required to correct the dehydration.

· Lactated Ringer's solution should be avoided as the liver eventually converts lactate to bicarbonate; because of potentially poor tissue perfusion, volume expansion with normal saline is safest.

· When plasma glucose reaches 250 mg/dL, an infusion of D₅W is added to the insulin infusion to decrease the possibility of hypoglycemia and to provide a continuous source of glucose and insulin for eventual normalization of intracellular metabolism.

· These patients may require a nasogastric tube for gastric decompression and bladder catheterization to monitor urinary output.

Acidosis

· Correction of severe acidosis (pH < 7.1) with bicarbonate is seldom necessary, as the acidosis corrects with volume expansion and with normalization of the hyperglycemia.

Hyperosmolar non-ketotic coma

Overview

· Ketoacidosis is not a feature of hyperosmolar nonketotic coma possibly because enough insulin is available to prevent ketone body formation.

· Instead, a hyperglycemic diuresis results in dehydration and hyperosmolality.

· Severe dehydration eventually leads to renal failure, lactic acidosis, and a predisposition to form intravascular thromboses.

· Hyperosmolality, frequently exceeding 360 mOsm/L, alters cerebral water balance, causing changes in mental status and seizures.

· Severe hyperglycemia causes a factitious hyponatremia: each 100 mg/dL increase in plasma glucose lowers plasma sodium concentration by 1.6 mEq/L.

Treatment

· Treatment includes fluid resuscitation with normal saline, relatively small doses of insulin, and potassium supplementation.

· Hypoglycemia in the diabetic patient is the result of an excess of insulin relative to carbohydrate intake.

· Furthermore, some diabetic patients are unable to counter hypoglycemia by secreting glucagon or epinephrine (counterregulatory failure).

· The dependence of the brain on glucose as an energy source makes it the organ most susceptible to episodes of hypoglycemia.

· If hypoglycemia is not treated, mental status changes can progress from lightheadedness or confusion to convulsions and permanent coma.

· Systemic manifestations of hypoglycemia result from catecholamine discharge and include diaphoresis, tachycardia, and nervousness.

· Most of the signs and symptoms of hypoglycemia will be masked by general anesthesia.

· Although normal plasma glucose levels are ill-defined and depend on age and sex, hypoglycemia can generally be considered to be levels of less than 50 mg/dL.

Treatment

· The treatment of hypoglycemia is the intravenous administration of 50% glucose (each milliliter of 50% glucose will raise the blood glucose of a 70-kg patient by approximately 2 mg/dL).

Preoperative assessment

· The pre-operative evaluation is necessary to know the metabolic, nutritional, electrolyte, cardiac, pulmonary and renal functions as well as the autonomic and peripheral nervous system status.

· If the cardiac disease is suggested by history and physical examination, the tests to detect the presence of ischemic heart disease can be helpful in preoperative assessment of the patient.

History

· Determine the type and duration of diabetes mellitus

· Determine the medication , nature , duration, compliance to treatment

· Adequacy of blood glucose controlrol as shown by glycosylated haemoglobin HbA1C level, value of > 9 % shows that inadeqauate control,

· Assessment of presence target oragan damage ie Questioning to elicit symptoms of ischemic cardiac, renal, and/or peripheral vascular disease, if any.

Cardiovascular

· hypertension, coronary artery disease, cerebrovascular disease, peripheral vascular disease, autonomic neuropathy by identifying orthostatic hypertension

· Diabetic  complication may alter the intraoperative cardiovascular response, with resultant hypotension and increased cardiac morbidity,

Renal system :

· Evaluation of renal disease involves estimation of blood urea, serum creatinine, creatinine clearance, and quantification of proteins in the urine.

· This assess the presence of diabetic nephropathy

Nervous system :

· peripheral neuropathy

Eyes :

· premature cataract,

· diabetic retinopathy

Implication of diabetes to anesthetic management

Acute problems

· acute complications of poorly treated diabetes mellitus ;

· osmotic diuresis  with dehydration

· Ketoacidosis

· Hyperosmolar non-ketotic hyperglycemia crisis

· These are medical emergency , need stabilization and resuscitation before surgery

Cardiovascular problem;

· Perioperative blood pressure control is difficult with wide fluctuations that necessitate close monitoring and treatment

Renal problem

· Diabetic nephropathy cause prolonged action or overdosage of drug that renally excreted

Nervous system problem

· Autonomic neuropathy give rise to delayed gastric emptying, perioperative hypothermia , postural hypotension, abnormal cardiac reflex, and silent myocardial inschemia

· Alterd levels  of conciousness secondary to hyperglycemia,hypoglycemia, cerebral insufficiency

· Assessment of nervous system and autonomic nervous system is specific, helps to be prepared for the post operative complications in a diabetic patient like gastroparesis, intestinal ileus and urinary retention.

Airway problem

· Thickening of soft tissues and joint immobility involving temporomandibular joints, atlanto-occipital joint, cervical spines cause difficult positioning and airway mnx

Electrolyte and metabolic problem

· Lactic acidosis secondary to anerobic metabolism worse the clinical outcome if ptn develop cardiac arrest of cerebral ischemia

Infection  problem

· Perioperative gm control is difficult

· Hyperglycemia ~~~>1. impaired wound healing, 2. deficient formation of granulation tissue,with poor tensile strength of collagen.

· The fibroblast formation takes longer time <> non-diabetics

· There is a deficient capillary growth into the wound.

· The chemotactic, phagocytic and bactericidal activity of the neutrophil is deficient.

· There is impaired humoral host defense mechanism and abnormal complement function

Infection problems

· Risk ofi nfection is high

· Woud healing is delayed in the presense of poor diabetic control

· Increase incident of chest infection if ptn is obese and smoker

Management of diabetic medication for major surgery

· The perioperative insulin requirements will be altered  as part of body stress response to sx

· This effects is persistent until ptn recovers from sx

· Therefore , the nature and dose of diabetic medication need to be adjusted accordingly

For type 1 , major sx

· The long acting insulin eq; crystalline insulin zinc suspension ; stopped and substitute with short or intermediate acting insulin

For type 2, major sx

· withold metformin at least  2 days before op;

· reason ; it can precipitate lactic acidosis

· Withold Chlorpropamide at least 3 days before op; reason ; duration of action is 36 hours

· If this is not possible , need frequent gm monitoring to exclude hypoglycemia

· For short acting oha eq; glibenclamide, may be substituted or change to s/c insulin

Perioperative management of diabetes mellitus

The nature and extent of medications depend on ;

· Elective or emergency

· The need for prolonged postoperative fasting ie > 24 hrs or major sx

· The postoperative fasting until ptn no nausea or vomiting ie minor sx

Perioperative plan

· Admit early for gm observation and stabilization

· Consult the  endocrinologist for co-management of blood glucose perioperative

· list ptn early or as first case to limit preoperative fasting time

· Close monitoring of blood sugar by gm or reagent strip, perform regularly, aim for gm 6-10

For minor surgery

Type 1

· Omit morning dose of insulin if blood glucose < 7 mmol/l

· Give half of normal dose if > 7 mmol/l

· Measure gm 1 hours before sx, at least once during sx, 2hrly postoperatively until ptn allow oral intake, then 4 hoursly

· Restart insulin once ptn taking orally

Type 2 minor sx

· If in diet control

· No special treatment if gm well controlled, diet treated patient

· If on hypoglycemia agents

· Omit morning dose of oha on the day of sx

· Gm 1 hour before sx, at least once intraoperatively, 2 hoursly postoperatively until taking orally , then 8 hoursly

· Restart oha once tolerate orally

Major sx

· Check gm and potassium preoperatively

· Omit insulin or oha on the day of sx

· Start iv infusion of dextrose 5% (500 ml over 4 hours) , or dextrose 10% (500 ml over 8 hours depending on fluid requirements

· Start variable-rate insulin infusion according to sliding scale insulin reqime

· Measure gm every 2 hours from the start of insulin sliding scale, then 1 hoursly intraoperatively , hoursly postoperatively for 4 hours, then every 2 hoursly

· Restart insulin or oha once ptn taking orally

Insulin infusion regime

· Various type

· most common;

· -GIK (glucose insulin potassium) or alberti regime

· -insulin according to sliding scale

advantages and disadvantage

· GIK (glucose insulin potassium) or alberti regime ; simpler, doesn't need infusion pump but less accurate glycemic control

GIK Regime

Preparation

· An amount of insulin is added to 500 ml dextrose 10 % according to gm

· 10 mmol/L of KCL is added to solution if k < 3.5 mmol/l

· This solution is given as infusion at 100 ml/hr

Regime

blood glucose concentration            insulin ( U)

 < 5                                                      omit

5- 10                                                     10

10- 15                                                   15

> 20                                                      20

Sding scale insulin regime

· Variable -rate infusion of insulin 50 u in 50 ml 0.9 % ns ie concentration 1 U/ml

· This infusion is adjusted according to blood glucose mmol/l

Gm

· < 5       omit

· 5-10       1

· 10-15     3

· 15-20     4

· > 20       5

emergency sx

· Management dillema; if urgent despite poor glycemic control , presense of sepsis foci ex abscess or infected diabetic gangrene that cause difficulty in glycemic control

· Need to be control by endocronologist, medical

· Need to correct; acidosis , dehydration, electrolyte imbalance preoperatively

· Blood glucose concentration up to 15 mmol/l may be accepted providing that the treatment is on-going.

Choice of anesthesia

· No evidence that any techniques is superior than the other

· Regional anesthesia ; more recommended

· Need to know that central neuroaxial blockade can cause profound hypotension in ptn with autonomic neuropathy

· SA a/w increased incidence of peripheral neuropathies

Monitoring

· extent of monitoringv depend on extent of sx, severity of systemic disease ex the presence of ihd, hypertension, nephropathy

· Poorly controlled diabetes need to have close monitoring if need large doses of insulin for satisfactory control  and adjusted accordingly

Induction

· Need to attenuate the stress response to sx.

· Stress response a/w; release of stress hormone, cathecholamine, other mediators that has deleteriousveffect on cvs

· urgery causes a considerable metabolic stress in the non-diabetic and more so in a diabetic.

· The stress response to surgery is mediated by neuroendocrine system essentially by stimulating the adreno-medullary axis.

· The neuro endocrine system aim to maintain fuel requirements by glycogenolysis and gluconeogenesis .

· these is achieve through stress hormones catecholamines, glucagon, cortisol, and growth hormone.

· In a non-diabetic there is enough Insulin secretion to utilize the fuel produced by the stress hormones and thus glucose homeostasis is maintained.

· Whereas this compensatory elaboration of insulin is less possible in Type II diabetic & cannot occur in Type I diabetic.

Airway management

· Problems ; Thickening of soft tissues and joint immobility involving temporomandibular joints, atlanto-occipital joint, cervical spines

· Effects ; difficult positioning, difficult laryngoscopy, intubation

· May need to do fibreoptic laryngoscopy , careful positioning, to prevent musculoskeletal and neurovascular injuries

Intraoperative glycemic control

· For minor sx; Majority don't require insulin supplement

· Avoid;

· -large fluctuations of blood glucose  level; both hypo, hyperglycemia are poorly tolerated

· -hyperglycemia results in hyperosmolarity, dehydration, osmotic diuresis

· -hypoglycemia in anesthetized ptn may lack warning sign; sweating, restlessness, abdominal pain, and major cerebral complications

· -sudden reduction of blood glucose may lead to severe hypokalemia and hypoglycemia

· Need to monitored closely the rate of insulin and glucose monitoring for satisfactory control