How is hypoglycemic shock recognized and treated intraoperatively?

·       Hypoglycemia can lead to tissue energy failure and has been associated with hemodynamic collapse and brain injury.

·       Any patient receiving insulin, pramlintide, sitagliptin, or sulfonylureas is at risk for hypoglycemia.

·       Because risk is usually known beforehand, hourly or more frequent monitoring of serum glucose should detect hypoglycemia.

·       If glucose levels are low or decrease rapidly, the fastest treatment is a bolus of intravenous dextrose, 50% solution, administered slowly.

·       In an emergency, one full ampule is the starting dose.

·       In less urgent settings when the serum glucose level is low but not critical, smaller doses can be titrated to serum glucose values.

D. Postoperative Management

D.1. How is diabetes controlled in this patient postoperatively?

·       Unless there is a change in disease status as a consequence of surgery or preoperative care was inadequate, this patient should be transitioned back to her preoperative regimen.

·       Before transitioning, she must recover from the stress response to the surgery.

·       If this were a simple outpatient procedure, such as a cataract extraction, she could return home on her outpatient medication regimen.

·       In this case, however, the effects of tissue injury may not peak for days; diabetes control is thus a dynamic challenge.

·       Regular monitoring of glucose is required (at a minimum checks should be made every 6 hours).

·       She is monitored for hyperglycemia, and her nutrition regimen is adjusted to serum glucose measurements.

·       Hourly glucose measurements and insulin infusion can control hyperglycemia.

·       Most patients can be effectively managed with subcutaneous insulin and less frequent measurements.

·       Insulin dose should take into account preoperative requirements, insulin resistance from the stress response, and caloric intake.

·       Many patients receive intravenous dextrose postoperatively; if they are hyperglycemic on this regimen, dextrose is discontinued.

D.2. Does diabetes increase perioperative risk?

·       Because patients with diabetes are at a greater risk of atherosclerosis, infection, autonomic and cardiovascular instability, and metabolic abnormalities than those without diabetes, perioperative risk is higher in this patient population.

·       After surgery, the diabetic patient is monitored for hyperglycemia and hypoglycemia, ischemic complications, circulatory compromise, and wound and nosocomial infection.

·       As a group, patients with diabetes have an increased risk for complications and poor outcomes from complications.

D.3. What are the common postoperative complications to be expected in a diabetic patient?

·       Hyperglycemia and hypoglycemia, wound infections, and organ ischemia are the most common and worrisome postoperative complications in patients with diabetes.

·       Following myocardial infarction or cerebrovascular accident, hyperglycemia is associated with a worse prognosis.

D.4. Is it necessary to achieve tight perioperative control of glucose?

·       In the critical care setting, there is evidence for improved outcomes with tight glycemic control, variably defined as serum glucose between 80 and 120 mg per dL or higher; other evidence has shown no benefit or even harm.

·       Some advocate for tight glycemic control in cardiac and noncardiac surgery.

·       The risks of hypoglycemia and data from more recent studies have tempered the enthusiasm for tight glycemic control.

·       Potential benefits from tight glycemic control include improvement in metabolic, anti-inflammatory, organ, and circulatory function.

·       Unfortunately, there is little evidence to suggest these benefits are substantial perioperatively.

·       Unresolved issues are the best time for tight control, the goals of therapy, the effect of nutrition, and the magnitude and factors in the potential for significant hypoglycemia.

·       The patient is transitioned to her preoperative level of control during recovery, and severe hyperglycemia is prevented by monitoring glucose closely.

·       Glucose levels above 180 mg per dL increase the risk of protein glycation and osmotic diuresis; targeting serum glucose below this value makes physiologic sense.

Protein glycation, diabetes, and aging.

·       Biological amines react with reducing sugars to form a complex family of rearranged and dehydrated covalent adducts that are often yellow-brown and/or fluorescent and include many cross-linked structures.

·       Food chemists have long studied this process as a source of flavor, color, and texture changes in cooked, processed, and stored foods.

·       During the 1970s and 1980s, it was realized that this process, called the Maillard reaction or advanced glycation, also occurs slowly in vivo.

·       Advanced glycation endproducts (AGEs) that form are implicated, causing the complications of diabetes and aging, primarily via adventitious and crosslinking of proteins.

·       Long-lived proteins such as structural collagen and lens crystallins particularly are implicated as pathogenic targets of AGE processes.

·       AGE formation in vascular wall collagen appears to be an especially deleterious event, causing crosslinking of collagen molecules to each other and to circulating proteins.

·       This leads to plaque formation, basement membrane thickening, and loss of vascular elasticity.

·       The chemistry of these later-stage, glycation-derived crosslinks is still incompletely understood but, based on the hypothesis that AGE formation involves reactive carbonyl groups,

·       Subsequent studies by many researchers have shown the effectiveness of aminoguanidine in slowing or preventing a wide range of complications of diabetes and aging in animals and, recently, in humans.

·       Since, the authors have developed a new class of agents, exemplified by 4,5-dimethyl-3-phenacylthiazolium chloride (DPTC), which can chemically break already-formed AGE protein-protein crosslinks.

·       These agents are based on a new theory of AGE crosslinking that postulates that alpha-dicarbonyl structures are present in AGE protein-protein crosslinks.

·       In studies in aged animals, DPTC has been shown to be capable of reverting indices of vascular compliance to levels seen in younger animals.

·       Human clinical trials are underway.