From American Diabetes Association: Diabetes Care 36(Suppl. 1):S13, 2013.
Hyperglycemia is most often cited as the primary problem with diabetes. However, it is usually the resultant long-term physiologic changes from hyperglycemia that cause the person with diabetes to require surgery. Hyperglycemia causes glycosylation, the binding of BG to proteins, which then impairs the function of the cells. Osmotic swelling occurs, resulting in cell damage to many of the body’s systems.12 Diabetes’ long-term complications are classified as macro- or microvascular. The most common of these include macrovascular complications of coronary artery disease, cerebrovascular disease, peripheral vascular disease, and microvascular complications including retinopathy, nephropathy, leg and foot ulcers, and autonomic neuropathy causing cardiac disease. It is estimated that those with diabetes have a 50% chance of requiring surgery in their lifetime13; most surgeries will be related to these complications.
Determination of any long-term complications and the level of BG control should be made in the preoperative period, hopefully weeks before the scheduled surgery through assessment, medical diligence, and intervention from the primary care physician (PCP) and/or the diabetes specialist. Input from medical records can also provide a more thorough assessment for the emergent surgical patient with diabetes. Results of a current A1C provide an overview of glucose control over the past 2 to 3 months; A1C values >7% have been shown to be a predictor of morbidity after coronary artery bypass graft (CABG) surgery.14 In a noncardiac surgical study, Underwood and others found that an A1C >8% increased the length of stay (LOS).15 They also found that 65% of persons preparing to undergo surgery had no A1C reported in the past 3 months.15
Preoperative Considerations
Preoperative guidelines for medications depend on the person’s home regimen and should be discussed with the person’s PCP and diabetes specialist before the surgical intervention. Varied combinations of medications prescribed make it difficult to find a standardized preoperative plan that works for all people with type 1 or type 2 DM. If possible, those with DM should be scheduled for an early morning surgery to reduce the time without oral intake and medications.13 Surgery involving children or adolescents should take place at a facility designated for that age group.16
In general, persons on oral medications or noninsulin injectables should be advised to hold those medications the evening before or the day of surgery primarily for prevention of hypoglycemia. Metformin is withheld to prevent the possibility of lactic acidosis (Table 48.3). Persons with type 1 DM may be advised to reduce the bedtime insulin to prevent hypoglycemia while NPO before surgery. However, some form of maintenance insulin must be continued to prevent hyperglycemia from the lack of basal insulin. Basal insulin is the amount of exogenous insulin per unit of time necessary to prevent hepatic gluconeogenesis and ketogenesis.
Table 48.3
Insulin Formulations Used in the Treatment of Diabetes
From DLife: Insulin Chart 2015. Available at http://www.dlife.com/diabetes/insulin/about_insulin/insulin-chart. Accessed August 20, 2016; Cahn A, et al.: New forms of insulin and insulin therapies for the treatment of type 2 diabetes. Lancet Diabetes Endocrinol 3: 638–652; 2015.
Those with type 1 are usually maintained on a basal dose of 1 or 2 injections of long-acting insulin, multiple injections of short or rapid insulin, or continuous subcutaneous insulin infusion (i.e., insulin pump with a rapid-acting analog).Refer to the individual hospital policies for details on use of an insulin pump in that facility. In general, the pump may be put into “suspend” mode for minor or short-duration surgeries. Longer procedures in which the person will have a longer period of sedation necessitates removal of the pump and implementation of an IV insulin drip. The bagged and labeled pump and equipment should be sent with the family and that action documented. Persons with type 2 DM who require insulin may also be instructed to reduce the bedtime insulin, but it is equally important that insulin be used to prevent hyperglycemia before surgery (Table 48.4).
Hyperglycemia Versus Hypoglycemia
Perioperative goals for the person with diabetes obviously include the universal positive outcomes sought for all surgical patients. For patients with DM and those with hyperglycemia but not diagnosed with DM, glycemic control is paramount, avoiding both hyperglycemia and hypoglycemia. The ADA defines hyperglycemia for all hospitalized patients as a BG > 140 mg/dL (7.8 mmol/L) regardless of a diagnosis of DM. Hypoglycemia is defined as a BG < 70 mg/dL (3.9 mmol/L) with or without symptoms.11 The balancing act of avoiding hyperglycemia while not triggering hypoglycemia proves to be difficult. Yet both have been shown to carry consequences if not controlled.
Up to 40% of those hospitalized will experience some degree of hyperglycemia.17 Surgery itself induces a stress response release of catecholamines, increasing glucagon and decreasing the insulin response resulting in insulin resistance.13 Inpatient BG should remain between 140 and 180 mg/dL (7.8 to 10 mmol/L).11 The intraoperative BG should remain <180 mg/dL (10 mmol/L).14 BG levels for the child with DM should remain between 90 mg/dL (5 mmol/L) and 180 mg/dL (10 mmol/L) during all surgical procedures.18 The ramifications with increased BG are many. Surgical site infections occur 2 to 3 times more often, and hyperglycemia impairs phagocytosis, delays chemotaxis, and depresses bactericidal capacity.12, 13 Persons with uncontrolled DM are at greater risk of poor wound healing, respiratory infection, myocardial infarction, the need for intensive care, and increased LOS.19 Despite these potential adverse outcomes, there are times when the quest for control of hyperglycemia is sacrificed in the attempt to avoid hypoglycemia.
Table 48.4
Oral Medications, Non-Insulin Injectable Medications for Persons With DM (combination compounds are not included)
| Chemical Class | Compounds | Action |
| Biguanides | Metformin | ↓endogenous hepatic glucose production, ↑peripheral glucose uptake |
| Sulfonylureas | Glipizide Glyburide Glimiperide | ↑secretion of insulin from beta cells |
| Meglitinides | Repaglinide Nateglinide | ↑secretion of insulin from beta cells |
| Thiazolidinediones | Pioglitazone Rosiglitazone | Improves insulin action in the periphery and the liver |
| α-Glycosidase inhibitors | Acarbose Miglitol | Inhibits intestinal α-glucosidase, delaying glucose absorption |
| GLP-1 receptor agonist–injectable | Exenatide Liraglutide Albiglutide Dulaglutide | Stimulates insulin secretion, facilitates homeostasis following food ingestion |
| Amylinomimetic-injectable | Pramlintide | Regulates glucose concentration post meal (PP), ↑satiety, slows gastric emptying, ↓glucagon secretion |
| DPP-4 inhibitors | Sitagliptin Saxagliptin Linagliptin Alogliptin | ↓endogenous hepatic glucose production, ↑secretion of insulin from beta cells |
| Bile acid sequestrants | Colesevelam | Poss. ↓endogenous hepatic glucose production, ↑incretin levels |
| Dopamine-2 agonist | Bromocriptine | Hypothalamic regulation–metabolism, ↑insulin sensitivity |
| SGLT2 inhibitors | Canagliflozin Dapagliflozin Emapgliflozin | Blocks glucose reabsorption in the kidneys, increasing glucosuria |
From American Diabetes Association: Diabetes Care 38:142–143, 2013.
If the preoperative BG is in the low normal range between 70 and 89 mg/dL (3.9 and 4.9 mmol/L), the risk of BG <70 mg/dL (3.9 mmol/L) or lower rises greatly. Possible causes for the lower BG should be determined before proceeding. Precipitating factors include heart failure, renal or liver disease, malignancy, infection, or sepsis.20 In an outpatient setting, an IV of 5% dextrose may prevent a decreasing BG. Therapy with 10% or 50% IV dextrose may be necessary to prevent subsequent perioperative hypoglycemia in the hospital. In the anesthetized person, detection of hypoglycemia depends on BG monitoring and physical indicators such as a decrease in blood pressure or an increased heart rate.21
Intraoperative Guidelines
The nature and duration of the surgical procedure affects the glucose level and the insulin interventions needed. Doses and frequency may be determined by the hospital or surgical center protocols. The relative insulin deficiency (type 2) and the absolute deficiency (type 1) require supplemental insulin IV or subcutaneous basal or bolus injections dependent on where the person is in the perioperative process. Insulin resistance rises during surgery but then rapidly decreases in the postoperative period, increasing the risk of hypoglycemia.22
Minor surgical procedures of short duration or persons receiving limited general, local, epidural, or spinal anesthesia may only need minimal changes in their diabetes regimen. Procedures of longer than 2 hours under general anesthesia will have greater glucose variations and require more frequent monitoring and treatment. IV regular insulin is used for glucose control during surgery to keep the patient’s BG <180 mg/dL (10 mmol/L).18 Subcutaneous insulin is not used during surgery because the absorption is affected by the person’s body temperature, circulating blood volumes, and certain anesthetics.
Postoperative Guidelines
Postoperative goals for the patient with DM include the universal outcomes of stabilizing vital signs, correcting fluid and electrolyte imbalances, preventing wound infection, and promoting wound healing. Patients with peripheral vascular disease and/or neuropathy require frequent skin inspection for signs of breakdown, pressure points, or shearing injuries to the skin. For all persons with DM or hyperglycemia, it will be necessary to include nutritional and correctional insulin (rapid or short acting) to the routine established in the surgical period. Nutritional insulin is the amount of exogenous insulin necessary to prevent hyperglycemia associated with any type of nutritional supplement such as discrete meals, total parenteral nutrition (TPN), and enteral feedings. Nutritional insulin is omitted if no food or caloric liquids are ingested. Correctional or supplemental insulin is used to correct unexpected hyperglycemia that occurs before or between meals.
Postoperative BG maintained at <180 mg/dL (10 mmol/L) reduced morbidity and mortality, decreased the rate of infection, reduced hospital LOS, and enhanced long-term survival.22 Detection of hypoglycemia depends on BG monitoring. Comprehensive hypoglycemia awareness involves having a plan for prevention as well as a plan for treatment. Hypoglycemia may be caused by the delay or omission of a meal, insulin overdose, or the improper timing of insulin and food. Prevention of severe hypoglycemia decreases hospital cost and lessens the likelihood of discharge to a skilled nursing facility, of having an increased LOS, and of greater mortality.21
Comprehensive diabetes control and the inherent BG control throughout the preparation for and completion of surgery determine the success of the procedure, the adverse or positive outcomes, and the overall continued health of that person. Diabetes control or the lack thereof affects us all. The American Diabetes Association released figures in 2013 stating that the cost of diagnosed diabetes rose from $174 billion in 2007 to $245 billion in 2012.11 Twenty percent of the nation’s health care dollars are funneled to diabetes care.23 Forty-three percent of the cost of diabetes stems from hospital inpatient care.15
The perianesthesia nurse’s impact on the outcomes for the person with diabetes is irrefutable. Assessment of the preoperative readiness, intraoperative BG control, and postoperative intervention for DM control influence that person’s health for months beyond the actual surgical intervention period. Perioperative nursing expertise and interventions can lower medical costs and increase the quality of life.
Research Needs
Further research should be conducted on patients with DM during the perioperative period. One example is a study of outcomes related to BG control for persons not requiring critical care postoperatively. Follow-up studies of patient outcomes once they have returned to the care of the surgeon or the PCP are needed but have been limited by the reluctance to report infections or other complications related to the surgery. More work is needed to determine outcomes of persons screened in preadmission testing who were found to have no A1C or to have hyperglycemia or an A1C >7% related to communication among providers.
Sickle Cell Disease
Sickle cell disease (SCD) is an inherited disorder of hemoglobin formation that leads to chronic hemolytic anemia, vaso-occlusive crises with severe pain, and progressive end organ damage. The mutated gene is transmitted by recessive inheritance and can manifest as sickle cell trait or SCD.5 SCD affects millions of people throughout the world and is most commonly associated with people of African descent, although the gene can be found in all ethnic groups. The exact number of Americans living with SCD is unknown; however, it is estimated that up to 100,000 people are affected. SCD is associated with significant morbidity and mortality, with an average life span of 45 years of age.24
Normally, adult blood is comprised of three different types of hemoglobin in erythrocytes: 96% to 98% hemoglobin A (HbA), 1% to 3% hemoglobin A2 (HbA2) and 0.5% to 0.8% fetal hemoglobin (HbF).25 The production of abnormal hemoglobin occurs due to a mutation on chromosome 11 with valine (amino acid) being substituted for glutamic acid. Whereas hemoglobin consists of four protein subunits (two of alpha-globin and two of beta-globin), this substitution of valine produces an abnormal beta-globin chain found in hemoglobin S (HbS). When HbS is exposed to adverse conditions of deoxygenation, these abnormal globin chains undergo polymerization and precipitation, leading to erythrocyte stiffness and distortion into a C-like shape similar to a sickle, thus the name of SCD. There are several different genotypes of SCD; however, in all the genotypes, HbS makes up at least half of the hemoglobin present. Variations in clinical presentation are in proportion to the concentration of HbS as it correlates with the risk of sickling. The replacement of both beta-globin subunits is found in patients diagnosed with homozygous sickle cell anemia. These persons have inherited sickling genes from both parents, and they usually have 80% to 95% HbS.5 Individuals heterozygous for the genes have the sickle cell trait and are carriers of SCD with virtually no symptoms.
The clinical manifestations are based entirely on sickling of the red blood cells and its consequences. Although the cell retains its ability to transport oxygen, it is stiff and misshapen with high susceptibility to destruction and deoxygenation as it passes through the splenic circulation. Sickling of red blood cells results from deoxygenation of HbS. It is important to note that the sickled cell may return to its normal shape with oxygenation; however, the cells will remain permanently sickled after repeated episodes of deoxygenation.
Two major consequences of sickling are chronic hemolytic anemia and blood vessel occlusion. Premature destruction of cells due to sickling occurs in the spleen. In people with SCD, the hemolysis and anemia from sickling result in a decrease in erythrocytes, with a mean life span of approximately 20 days compared with the normal 120 days.5 Erythrocytes that are sickled do not replace quickly enough, which results in a lack of oxygen circulating throughout the body. The byproducts from hemolysis can also lead to hyperbilirubinemia and jaundice, with many patients experiencing gallstones. Individuals with SCD routinely experience fatigue, pale skin, shortness of breath, and palpitations due to chronic hemolytic anemia.
Vaso-occlusive crisis in patients with SCD can be precipitated by cold, infection, hypoxia, dehydration, and stress. Another consequence of sickling, vaso-occlusion is a complex process initiated by the adherence of sickled cells to vessel endothelium that causes activation of an inflammatory response with mediators and other substances increasing platelet aggregation and promotion of blood coagulation.5 Because of increased viscosity and deformed red blood cells, the sickled cells wedge in the capillary bed and occlude normal flow. Vessel occlusion and the accompanying inflammation cause tissue ischemia and a vaso-occlusive pain crisis. The acute pain results from tissue hypoxia and infarction. Common sites obstructed by sickled cells are the abdomen, chest, bones, and joints. Years of tissue infarctions cause chronic damage to the liver, spleen, heart, kidneys, retinas, and other organs and eventual organ failure.
Other types of SCD crises that may occur include the aplastic and sequestration crises. The aplastic crisis is most grave and constitutes a medical emergency. It is characterized by a sudden drastic decrease in red blood cell production. The patient initially appears weak and has signs of cardiac decompensation. In a sequestration crisis, a large amount of blood becomes trapped in the spleen and causes hypovolemia and shock, which constitutes a medical emergency.
Surgical Considerations
The perianesthesia period is a time of increased risk for patients with SCD, and even though patients may present for minor surgery, it is common for patients to have surgery related to the disease such as cholecystectomy, splenectomy, or joint replacement. Many factors known to precipitate sickling can be encountered during the surgical experience; thus careful attention to detail is essential to avoid SCD crisis. The perianesthesia nurse needs to be aware that causes of sickling and vessel occlusion include situations that cause stress, acidosis, hypoxia, hypothermia, or dehydration. There are several factors that may also increase the risk of postoperative complications such as HbS level, preoperative blood transfusion, type of anesthesia, emergent versus elective surgery, type of surgery, and open versus laparoscopic surgery. The care of patients with SCD needs to be multidisciplinary in approach to personalize the plan of care for the best outcome possible.
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