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Anesthesia & DiabetesAnesthesia & Diabetes Dr Jarahzadeh Dr Jarahzadeh(Intesivist)(Intesivist)

DIABETES MELLITUS Normal glucose physiology demonstrates a balance between glucose utilization and endogenous production or dietary delivery

The liver is the primary source of endogenous glucose production via glycogenolysis and gluconeogenesis .

Following a meal, plasma glucose increases, which stimulates an increase in plasma insulin (maximum insulin level is reached

within 30 minutes) promoting glucose utilization .Late in the postprandial period (2–4 hours after eating), the plasma glucose concentration decreases to below the fasting level

before returning to preprandial values .A transition from exogenous glucose delivery to endogenous production then becomes necessary to maintain a normal plasma glucose level. During the postabsorptive phase (4–8 hours after eating) plasma glucose remains relatively stable with production and utilization rates being equal. At this time, 75% of glucose production results from hepatic glycogenolysis and 25% from hepatic gluconeogenesis .

Approximately 70% to 80% of glucose released by the liver is metabolized by insulin-insensitive tissues such as the

brain, gastrointestinal tract, and red blood cells .During this time, diminished insulin secretion is fundamental to the maintenance of a normal plasma glucose concentration.

Hyperglycemia-producing hormones (glucagon,epinephrine, growth hormone, cortisol)

Glucagon plays a primary role by stimulating glycogenolysis, gluconeogenesis, and inhibiting glycolysis .

Epinephrine predominates when glucagon secretion is deficient .

Neural glucoregulatory factors ( norepinephrine) and glucose autoregulation also support glucose production.

Type 1 Diabetes Five percent to 10% of all cases of diabetes are type 1. It is usually diagnosed before the age of 40 years and is one of the most common chronic childhood illnesses.

Type 1 diabetes is caused by a T cell–mediated autoimmune destruction of beta cells of the pancreas .

The exact etiology is unknown, although environmental triggers such as viruses (especially enteroviruses), dietary proteins, and drugs/chemicals may initiate the autoimmune process in genetically susceptible hosts.

At least 80% to 90% of beta-cell function must be lost before hyperglycemia occurs.

Patients demonstrate hyperglycemia over several days to weeks associated with fatigue, weight loss, polyuria, polydipsia, blurring of vision, and signs of fatigue, weight loss, polyuria, polydipsia, blurring of vision, and signs of

intravascular volume depletionintravascular volume depletion . .

The diagnosis is based on the following symptoms: a random blood glucose greater than 200 mg/dL and a hemoglobin (Hb) A1c level greater than 7.0% .

The presence of ketoacidosis indicates severe insulin deficiency and unrestrained lipolysis. Beta-cell destruction is complete within 3 years of diagnosis in most young children, with the process being slower in adults

Type 2 Diabetes Type 2 diabetes is responsible for 90% of all cases of diabetes mellitus in the world.. Type 2 diabetics are typically in the middle to older age group and overweight,

It is estimated that most type 2 diabetics have had the disease for approximately 4 to 7 years before it is diagnosed.

Type 2 diabetes is characterized by relative beta-cell insufficiency and insulin .resistance

There are three important defects in type 2 diabetes :*increased rate of hepatic glucose release ,

*impaired basal and stimulated insulin secretion* inefficient use of glucose by peripheral tissues ( insulin resistance) .

Type 2 diabetes is characterized by insulin resistance in skeletal muscle, adipose tissue, the liver. Insulin resistance is defined as a less-than-normal biologic response to a given concentration of insulin.

Causes of insulin resistance include an abnormal insulin molecule, circulating insulin antagonists including counterregulatory hormones, free fatty acids, anti-insulin and insulin receptor antibodies and cytokines, and target

tissue defects at insulin receptors and/or postreceptor sites .

Metabolic syndromThe metabolic syndrome or insulin-resistance syndrome is a constellation of clinical and biochemical characteristics frequently seen in patients with or at risk of type 2 diabetes.

Diagnostic criteria for diabetes mellitus Diagnostic criteria for diabetes mellitus A normal fasting plasma glucose is 70 to 100 mg/dL. Hyperglycemia not sufficient to meet the diagnostic criteria for diabetes is classified as either impaired fasting glucose or impaired glucose tolerance, depending on whether it is identified through a fasting plasma glucose or an oral glucose tolerance Any fasting glucose between 101 and 125 mg/dL is impaired fasting glucose. the oral glucose tolerance test is recommended for diagnosis when

glucose values are equivocal .

The Hb A1c test provides a valuable assessment of long-term glycemiccontrol .

Erythrocyte hemoglobin is nonenzymatically glycosylated by glucose that freely crosses red blood cell membranes. The percentage of hemoglobin molecules participating in this reaction is proportional to the average plasma glucose concentration during

the preceding 60 to 90 days .

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%.

Venous plasma or serum is the standard body fluid for glucose determinations .

Arterial and capillary blood yield glucose values approximately 7% higher than venous blood .

Whole blood determinations are usually 15% lower than plasma or serum values .

Urine glucose is a poor diagnostic test since the renal glucose threshold is not reached until the extracellular glucose concentration exceeds 180 mg/dL. concentrations.

TreatmentTreatment

The cornerstones of therapy for type 2 diabetes are 1-diet with weight loss

2 -exercise therapy3-the oral antidiabetic agents .

The initial decrease in fasting plasma glucose results from a decrease in hepatic glycogen stores and a decline in glycogenolysis .

The decrease in adiposity improves hepatic and peripheral tissue insulin sensitivity, enhances post receptor insulin action, and may possibly increase insulin secretion.

Estimation of basal energy requirements and activity level requirements plus additional adjustments for growing children,

pregnancy, lactation, infection, illness, and surgery are necessary .Low-calorie diets (800–1500 kcal) and very low calorie diets (<800 kcal) with limits on cholesterol raising fats and added sugars are used to reduce body fat and decrease insulin resistance and to normalize plasma glucose, lipids, and lipoproteins.

Oral Antidiabetic AgentsOral Antidiabetic Agents The four major classes of oral agents are the secretagogues *sulfonylureas, meglitinides (Glibenclamid),which increase insulin availability.

*biguanides (metformin), which suppress excessive hepatic glucose release .

*Thiazolidinediones or glitazones (rosiglitazone pioglitazone), which improve insulin sensitivity

*α-glucosidase inhibitors (acarbose, miglitol), which delay gastrointestinal glucose absorption

These agents, either as monotherapy or in various combinations, are used to maintain glucose control (fasting glucose, 90–130 mg/dL; peak postprandial glucose( <180 mg/dL, Hb A1c <7%)in the initial stages of the disease

InsulinInsulin Insulin is necessary to manage all type 1 diabetics

and many type 2 diabetics. In the United States, 30% of type 2 diabetics are

treated with insulin .Conventional insulin therapy uses twice-daily

injections .*Intensive insulin therapy uses three or more daily

injections or a continuous infusion .

The various forms of insulin include basal insulins, which are intermediate acting (NPH, lente, lispro protamine, aspart protamine) and administered twice daily

or long acting (ultralente and glargine) and administered once daily,

and insulins that are short acting (regular) or rapid acting (lispro, aspart), which provide glycemic control at mealtimes (prandial insulin) .

Conventional insulin therapy usually requires twice-daily injections of combinations of intermediate-acting and short-/rapid-

acting insulins such as Humulin 70/30 insulin (70% NPH, 30%

regular), Novolog 70/30 (70% insulin aspart protamine plus 30%

insulin aspart) or Humalog 75/25 (75% insulin lispro protamine plus 25% insulin lispro).

For Humulin For Humulin 70/30, injections are given 30 minutes before breakfast and 30 minutes before dinner .

For Novalog 70/30 and Humalog 75/25For Novalog 70/30 and Humalog 75/25, injections are given 5 to 15 5 to 15 minutes before breakfast and 5 to 15 minutes before dinner .

Twice-daily separate injections of NPH insulin and regular insulin or NPH insulin and rapid-acting insulin (lispro, aspart) are another conventional method of administration

Intensive insulin therapy uses three or four daily injections or a continuous infusion with more frequent glucose monitoring .

Three daily injections includes NPH plus short-acting (regular) or rapid-acting (lispro, aspart) insulin before breakfast, short-acting or rapid-acting insulin before

dinner, and NPH insulin at bedtime. Four daily injections can include a single injection of NPH, lente, or insulin glargine (Lantus) at bedtime plus short-acting or rapid-acting insulin before breakfast, lunch, and dinner .A subcutaneous infusion pump uses regular or rapid-acting insulin with a usual range of 0.5 to 2.0 units per hour.

A typical total daily basal dose of insulin equals weight (kg) × 0.3, with the hourly rate obtained by dividing by 24 .

Basal rates vary during a 24-hour period with lower rates required at bedtime, higher rates between 3 and 9 AM and

intermediate rates during the day. Premeal boluses may also be used, and insulin rates must be adjusted for

exercise .Ideal glycemic goals for type 1 diabetics include the following: before meals, 70 to 120 mg/dL; after meals, less than 150 mg/dL; at bedtime, 100 to 130 mg/dL; and at 3:00 AM more than 70 mg/dL.

For many type 2 diabeticsFor many type 2 diabetics ,early and aggressive initiation of insulin therapy has demonstrated beneficial effects. Reports of remissions of type 2 diabetes with early intensive insulin treatment suggests that it should be prescribed early rather than as a treatment of last resort. Unlike oral agents, insulin has no upper dose limit and can be adjusted over time to achieve near-normal glucose levels. Many type 2 diabetics require 0.6 to 1.0 U/kg per day. The amount of insulin needed is not related to the degree of hyperglycemia but to body adiposity and other factors of insulin resistance. In most studies, obese type 2 diabetics require significant daily doses (100–200 units) to achieve near-normal glycemia .

Fortunately, blood glucose levels for type 2 diabetics are much less labile than for type 1 diabetics and adjustment of the dose is less necessary.

Insulin therapy is usually initiated with 10 to 15 units of intermediate-acting insulin at bedtime with the dose being adjusted until fasting levels are therapeutic, or, alternatively, administering long-acting insulin glargine in the evening. If glucose levels remain elevated during the day, intermediate-acting insulin is added in the morning with or without short- or rapid-acting insulin. Type 2 diabetics who benefit most from insulin therapy are those who demonstrate catabolism with ketonuria, persistently elevated glucose levels despite oral therapy, severe hypertriglyceridemia, uncontrolled weight loss or severe dehydration with hyperglycemia, or the desire to maintain near-normal glycemia or induce remission

Hypoglycemia is the most frequent and dangerous complication of insulin . Approximately 30% of type 1 diabetics experience one or more severe hypoglycemic attacks per year.

The incidence is three times higher in the intensive therapy group than the conventional group .

The hypoglycemic effect can be exacerbated by simultaneous administration of alcohol, sulfonylureas, biguanides, thiazolidinediones, angiotensin-converting enzyme (ACE) inhibitors, monoamine oxidase inhibitors, and nonselective β-blockers.

β-Blockers may exacerbate hypoglycemia by inhibiting adipose tissue lipolysis, which serves as an alternate fuel when patients become hypoglycemic .

Defective counterregulatory responses by glucagon and epinephrine to reduced plasma glucose levels contribute to this complication .

Repetitive episodes of hypoglycemia, especially at night, results in hypoglycemia unawareness where the patient does not respond with the appropriate autonomic warning symptoms before neuroglycopenia.

The diagnosis in adults requires a plasma glucose level less than 50 mg/dL. Symptoms are adrenergic (sweating, tachycardia, palpitations, restlessness, pallor) and neuroglycopenic (fatigue, confusion, headache, somnolence,

convulsions, coma) .Treatment, if conscious, includes the administration of sugar in the form of sugar cubes, glucose tablets or soft drinks, and, if unconscious, glucose 0.5 g/kg IV or glucagon 0.5 to 1.0 mg IV, IM, or SC

Diabetic KetoacidosisDiabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a complication of decompensated diabetes mellitus .

The signs and symptoms of DKA are primarily the result of abnormalities in carbohydrate and fat metabolism.

Episodes of DKA occur more commonly in type 1 diabetics and are precipitated by infection or acute illness (cerebrovascular accident, myocardial infarction, acute pancreatitis)

High glucose levels exceed the threshold for renal tubular absorption creating a significant osmotic diuresis with marked hypovolemia

Hyperglycemic Hyperosmolar SyndromeHyperglycemic Hyperosmolar Syndrome

Hyperglycemic hyperosmolar syndrome (HHS) is characterized by severe hyperglycemia, hyperosmolarity, and dehydration usually in elderly (older than 60 years) type 2 diabetics who live alone, are socially isolated, and experience an acute illness such as infection, myocardial infarction, cerebrovascular accident, pancreatitis, intestinal obstruction, endocrinopathy, renal failure, or a burn.

The patient presents with polyuria, polydipsia, hypovolemia, hypotension, tachycardia, and organ hypoperfusion .

The early administration of large volumes of crystalloid fluids is necessary to prevent this syndrome. Hyperosmolarity (>340 mOsm/L) is responsible

for an obtunded mental status or coma .

Patients may have some degree of metabolic acidosis but do not demonstrate a ketosis .

Vascular occlusions secondary to 1-mesenteric artery thrombosis

2 -low-flow states3-DICDIC (Diffuse intravascular coagulation)

Glycemic ControlGlycemic Control Controlled clinical trials and epidemiologic studies have analyzed the relationship between the degree of glycemic control and the

incidence of microvascular and macrovascular complications .

Randomized, controlled clinical trials have unequivocally established that strict control of glycemia can decrease the risk of microangiopathic (nephropathy, peripheral neuropathy,

retinopathy) complications of diabetes .

Microvascular dysfunction is characterized by Nonocclusive, microcirculatory impairment with vascular

permeability and impaired autoregulation of blood flow and vascular tone.

Intensive glycemic control Intensive glycemic control (near normal range) delays the onset and slows progression of microvascular effects, demonstrating significant improvements in all outcomes for all microvascular complications .

The major morbidity and mortality from type 2 diabetes

is secondary to accelerated atherosclerosisaccelerated atherosclerosis, a multifactorial disease multifactorial disease process not solely due to hyperglycemia .

As a result, treatment must be directed at multiple risk factors in addition to hyperglycemia such as hypertension, hyperlipidemia, hypertension, hyperlipidemia,

and smokingand smoking . .A growing number of epidemiologic studies have demonstrated an association between the degree of glycemia and macrovascular (cardiovascular, cerebrovascular, and peripheral vascular disease) complications, but large randomized clinical trials have not convincingly shown that macrovascular disease is affected by

glycemic control .The macrovascular pathology is morphologically and functionally similar to nondiabetics and is characterized by atherosclerotic atherosclerotic lesions of the coronary and peripheral arterial circulationslesions of the coronary and peripheral arterial circulations.

Microvascular Complications

**RetinopathyRetinopathy

****NephropathyNephropathy

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Visual Complications of Diabetes

Diabetic retinopathy can lead to blindnesDiabetic retinopathy can lead to blindnes

Education of client *Check blood sugar

*Check blood pressure*Regular eye exam with ophthalmologist

*Laser photocoagulation therapy

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Management of AnesthesiaManagement of Anesthesia

The goals of anesthetic management of the diabetic patient include

*preoperative evaluation .

*An in-depth understanding of the pathophysiology of diabetes and the metabolic stress response .

*Asignificant knowledge and understanding of insulin, and possibly collaboration with the patient’s internist/endocrinologist .

Management of AnesthesiaManagement of Anesthesia .The stress response of surgery

1-Activation of the sympathetic nervous system and release of catecholamines, cortisol, and growth hormone may be sufficient to convert a well-controlled

diabetic to one with significant hyperglycemia and even ketoacidosis ,

2-Reduction in insulin sensitivity (insulin resistance of surgery) in the periphery The magnitude of surgery is very important, with major surgery creating

significant metabolic derangements and minor surgery demonstrating less risk .

The effects of chronic hyperglycemia The effects of chronic hyperglycemia ((coronary artery disease, myocardial coronary artery disease, myocardial infarction, congestive heart failure, peripheral vascular disease, hypertension, infarction, congestive heart failure, peripheral vascular disease, hypertension, cerebrovascular accident, chronic renal failure, infection, neuropathycerebrovascular accident, chronic renal failure, infection, neuropathy) ) are frequently present on preoperative evaluation and should be medically optimized

before proceeding ,

The effects of acute hyperglycemia The effects of acute hyperglycemia are also dangerous and must be managed

Management of AnesthesiaManagement of Anesthesia

Acute and chronic hyperglycemia appear to Increase the risk of ischemic myocardial injury by decreasing coronary collateral

blood flow and coronary vasodilator reserve, impairing coronary microcirculation and causing endothelial dysfunction .

Acute hyperglycemia causes

* Dehydration ,*Impaired wound healing ,

*increased rate of infection ,*Worsening central nervous system/spinal cord injury with ischemia ,

* Hyperviscosity with thrombogenesis .

Tight control Tight control of serum glucose in the perioperative period is important in managing the consequences of acute and chronic hyperglycemia.

Management of AnesthesiaManagement of Anesthesia Preoperative Evaluation The preoperative evaluation should emphasize

the cardiovascular, renal, neurologic, and musculoskeletal systemsthe cardiovascular, renal, neurologic, and musculoskeletal systems. A high index of suspicion should exist for myocardial ischemia and infarction .

Silent ischemia Silent ischemia is possible if an autonomic neuropathy is present.

Stress testing should be considered if a patient exhibits two or more cardiac risk factors and is undergoing major surgery

ββ11-Antagonists-Antagonists should be used if coronary artery disease is present to decrease morbidity and mortality perioperatively .

For renal diseaseFor renal disease, control of hypertension hypertension is a major priority, using ACE ACE inhibitors .

Meticulous attention to hydration status, avoiding nephrotoxinsnephrotoxins, and preserving renal blood flow are also essential .

Management of AnesthesiaManagement of Anesthesia Preoperative Evaluation

The presence of an autonomic neuropathy *Perioperative dysrhythmias .*Intraoperative hypotension .

*Gastroparesis with possible aspiration.* Hypoglycemia unawareness .

Preoperative evaluation of the musculoskeletal system limited joint mobility of the neck (nonenzymatic glycosylation of proteins and abnormal cross-linking of collagen). Firm, woody, nonpitting edema of the posterior neck and upper back (scleredema of diabetes) coupled with impaired joint mobility limits complete range of motion of the neck and may render endotracheal intubation Atleto-occipital)Atleto-occipital)).).difficult

Management of AnesthesiaManagement of AnesthesiaInsolin ThrapyInsolin Thrapy Management of insulin in the preoperative period depends on the

type of insulin that the patient takes and the timing of dosing . *If a patient takes subcutaneous insulin each night at bedtime, two

thirds of this dose (NPH and regular) should be administered the night before surgery and one half of the usual morning NPHNPH dose should be given on the day of surgery. The daily morning dose of

regular insulin should be held .A 5% dextrose with 0.45% normal saline (DA 5% dextrose with 0.45% normal saline (D55 ½ NS) intravenous ½ NS) intravenous

infusion at 100 mL/hr should be initiated preoperativelyinfusion at 100 mL/hr should be initiated preoperatively . .If the patient uses an insulin pump, the overnight rate should be decreased by 30% so that the patient receives 70% of the basal rate. On the morning of surgery, the pump can be kept infusing at the basal rate or discontinued and replaced with a continuous insulin infusion at the same rate, or the patient can be given subcutaneous GlargineGlargine and the pump discontinued in 60 to 90 60 to 90 minutesminutes

If the patient uses glargine and lispro or aspart for daily glycemic control, the patient should take two thirds of the glargine dose and the entire lispro or

aspart dose the night before surgery and hold all morning dosing.

Oral hypoglycemics should be discontinued 24 to 48 hours preoperatively. The sulfonylureas should also be avoided during the entire perioperative period since they block myocardial potassium ATP channels, which are responsible for

ischemia- and anesthetic-induced preconditioning .Well-controlled type 2 diabetics do not require insulin for minor surgery .

Poorly controlled type 2 diabetics and all type 1 diabetics having minor surgery and all diabetics having major surgery need insulin.

For major surgery, if the serum glucose is greater than 270 mg/dL preoperatively, the surgery should be delayed while rapid control is achieved with

intravenous insulin .

If the serum glucose is greater than 400 mg/dL, the surgery should be postponed and the metabolic state restabilized

Management of AnesthesiaManagement of Anesthesia Insolin Thrapy Insolin Thrapy

Intraoperative ManagementIntraoperative Management Two major goals are to minimize hyperglycemia and avoid hypoglycemia.

Ideally, a continuous infusion of insulin should be initiated at least 2 hours before surgery .

A sliding scale with short-acting, subcutaneous insulin for glucose greater than 200 to 250 mg/dL is

ineffective and should not be used .Intraoperative serum glucose levels should be

maintained between 120 and 180 mg/dL .Levels above 200 mg/dL are likely to be detrimental in the perioperative period,causing glycosuria and dehydration and inhibiting phagocyte function and

wound healing .

Intraoperative ManagementIntraoperative Management •Typically, one unit of insulin lowers glucose approximately 25 to

30 mg/dL .The initial hourly rate for a continuous insulin infusion is determined

by dividing the total daily insulin requirement by 24 .A typical rate is 0.02 U/kg per hour or 1.4 U/hr in a 70-kg patient .

An insulin infusion can be prepared by mixing 100 units of regular insulin in 100 mL NS (1 U/mL) .

Insulin infusion requirements are higher for CABG (0.06 U/kg per hour) ,patients receiving steroids (0.04 U/kg per hour) ,patients with severe infection (0.04 U/kg per hour) ,

patients receiving hyperalimentation or vasopressor infusions. Insulin infusions should be accompanied by an infusion of D5 ½ NS with 20 mEq KCl at 100 to 150 mL/hr to provide carbohydrate (at least 150 g/day) to inhibit hepatic glucose production and protein catabolism

Intraoperative ManagementIntraoperative Management

Serum glucose should be monitored every 1 hour and every 30 minutes for CABG or for patients with higher insulin requirements .

Spot urine glucose monitoring is not reliable, although the urine can be tested for ketones if the glucose increases to more than 250 mg/dL. For serum glucose values less than 100 mg/dL, the D5 ½ NS

infusion rate should be 150 mL/hr ;for (100 to 150 mg/dL), it should be 75 mL/hr ;for (151 to 200 mg/dL), it should be 50 mL/hr ,

for more than 200 mg/dL, a keep vein open (KVO) rate should be used.

Hypoglycemia is defined as a serum glucose less than 50 mg/dL in adults and 40 mg/dL in children .

Treatment consists of 50 mL of 50% dextrose (D50), which increases the glucose 100 mg/dL or 2 mg/dL/mL

Emergency Surgery Emergency surgery places diabetics at risk of developing DKA or HHS. Surgery should be delayed for 4 to 6 hours to optimize the patient’s metabolic status. DKA is more likely to develop in type 1 diabetics and is usually precipitated by IInfection, gastrointestinal obstruction, or trauma in the surgical patient. nfection, gastrointestinal obstruction, or trauma in the surgical patient. Patients present with hyperglycemia, hyperosmolarity, significant Patients present with hyperglycemia, hyperosmolarity, significant dehydration, ketosis, and acidosis. dehydration, ketosis, and acidosis.

TreatmentTreatment of of DKADKA includes includes large volumes of normal saline and insulin. An insulin bolus o.1 U/kg followed by an infusion of 0.1 U/kg per hour is the initial prescription. Serum glucose is monitored hourly, and electrolytes are monitored every 2 hours. Potassium, magnesium, and phosphate deficits are replaced when urine production is documented. When serum glucose decreases to less than 250 mg/dL, intravenous fluids should include dextrose. Insulin is continued until acidosis resolves.

Sodium bicarbonate is not routinely given and is reserved for cases

where the pH is less than 7.10

HHS usually occurs in elderly, debilitated type 2 diabetics. These patients present with greater metabolic derangements than those with DKA and are severely dehydrated ∼ 7-10 L hyperosmolar < 320 mOsm/L), and hyperglycemic < 800-1000 mg/dL. They may present with confusion, focal central nervous system deficits, seizures, or coma. Surprisingly, electrolyte deficits (K+,Mg2+ (are less severe than in DKA.Treatment consists of larger volumes of normal saline and similar doses of insulin compared to patients with DKA. These patients are at significant risk of developing of cerebral edema and therefore correction of serum glucose and osmolarity should proceed gradually over a 12 to 24 hour period

Emergency Surgery

Postoperative Care Aggressive insulin therapy in the intensive care unit (ICU) has demonstrated significant benefit in morbidity and

mortality .Patients receiving conventional insulin therapy (serum glucose, 180–200 mg/dL) demonstrate significantly higher rates of ICU mortality, in-hospital mortality and morbidity including sepsis, renal failure, and anemia sepsis, renal failure, and anemia than patients who

were tightly controlled (80–110 mg/dL) .Possible reasons for improved outcome in the latter include better neutrophil and macrophage function, beneficial changes to mucosal/skin barriers, enhanced erythropoiesis, reduced cholestasis, improved respiratory muscle function, and decreased axonal degeneration.

Postoperative Care

The postoperative management of diabetics requires meticulous monitoring of insulin requirements .

To determine the discharge dose, the total insulin (long, intermediate, short, rapid acting)

dose for the most recent 24-hour period is calculated, and 50% of the discharge dose is prescribed as long- or intermediate-acting insulin and 50% as short- or rapid-

acting insulin .If glargine is prescribed, it is usually given once at bedtime.

If the patient takes intermediate-acting insulin twice daily, then two thirds of the dose should be taken in the morning and one third at bedtime.

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