Hyperglycemia can potentially increase morbidity and mortality rates in surgical patients through cellular and biochemical changes.
Hyperglycemia leads to neutrophil dysfunction, activates blood coagulation, induces inflammation, depresses intrinsic myocardial protective mechanisms.1
According to the Society of Ambulatory Anesthesia, the optimal intraoperative glucose level is 180mg/dL or less. Surgery may proceed if patient presents with moderate hyperglycemia, but with evidence of adequate long-term glycemic control.
Providers may consider postponing surgery if hyperglycemia complications are noted, including dehydration ketoacidosis and hyperosmolar non-ketoacidosis. Furthermore, patients with chronically elevated hyperglycemia should not be acutely normalized during the perioperative period.2
Although the intraoperative guideline for minimum glucose requirement is not clearly defined, it can be assumed that the patient should at least be above the level of hypoglycemia or greater. Hypoglycemia is defined as a glucose level of below 70 mg/dL.
In fact, stringent intraoperative control has not been shown to improve patient outcomes. In a randomized controlled study of 399 patients who underwent on-pump cardiac surgery, patients who had received intensive insulin therapy with an intraoperative glucose target of 80 mg/dL to 100 mg/dL did not have reduced perioperative mortality or morbidity compared with the conventional group of patients who were not treated unless intraoperative glucose is greater than 200.3
The goal of preoperative glycemic optimization is to prescribe a regimen to achieve acceptable glucose control leading up to surgery. Individuals with long-term controlled or near-controlled preoperative glycemia require little or no change to their regimen (such as in the case of Mr. Q) while individuals with persistent severe hyperglycemia will require sequential medication titration with glycemic goal toward euglycemia.
Regardless of their baseline glycemic control or outpatient antihyperglycemic regimen, all patients will need guidance on how to revise their antihyperglycemic regimen up to 24 hours prior to surgery due to the withholding of nourishment by mouth at least eight hours prior to the procedure.
It is important to understand the concept of basal bolus insulin when dosing for proper preoperative glycemic management. Basal insulins such as insulin glargine, insulin detemir, and NPH (neutral protamine Hagedorn) refer to insulin use for control of glucose in the fasting state. Bolus insulin such as aspart, lispro, and regular includes prandial and correctional insulins.
Prandial insulin refers to insulin used for control of glucose in the presence of nutritional intake. Correctional insulin refers to insulin used when there is an underestimation of insulin requirement within the scheduled regimen used for the fasting state, nutritional intake or secondary to acute illnesses.4
When developing a preoperative glycemic control regimen, providers must account for the patient’s basal insulin need while in the fasting state, thus reducing the risk of hypoglycemia and preventing other perioperative complications associated with use of antihyperglycemic agents.
For example, biguanides such as metformin can induce lactic acidosis, a rare but potentially fatal condition, especially in the setting of comorbid renal insufficiency, heart failure, hypovolemia, and hypoxemia.
Sulfonylureas such as glyburide, glipizide, and glimepiride, are different class of oral antihyperglycemic agents that cause closure of cardiac potassium-dependent ATP channels, which may increase myocardial ischemia.1
It is critical to differentiate between basal insulin requirement and basal insulin dose when devising a preoperative antihyperglycemic regimen.
A patient may be taking a certain dose of basal insulin such as Lantus (glargine), but the dose can be greater than the patient’s basal insulin requirement and actually be used to manage prandial insulin requirement as well.
This is clearly evident in a patient who only uses basal insulins such as Levemir (detemir) but may not be too obvious in other regimens involving a basal insulin and multiple oral agents. For this reason, guidelines for dosing of preoperative insulins are usually given as a percentage range of the outpatient dose. The prescriber will still need to use his or her clinical judgment in order to recommend the most appropriate dose.
There are some differences between recommendations from national professional organizations on preoperative dosing of antihyperglycemic medications. However, there is consensus on withholding oral antihyperglycemic agents during the perioperative period with variable timing.
Generally for biguanides and sulfonyurea, hold 24 hour prior to surgery or day of surgery. For DPP4 inhibitors such as sitagliptin and linagliptin, thiazolidinediones such as pioglitazone and rosiglitazone and sodium-glucose cotransporter-2 inhibitors such as canagliflozin, and dapagliflozin, hold day of surgery.
The guidelines on preoperative antihyperglycemic injectables differs somewhat, but there is consensus on holding of prandial insulin and noninsulin injectables the day of surgery.
For peakless basal insulin, recommend 50% to 100% of usual dose, intermediate basal insulin 75% of evening dose, 50% of morning dose, premix insulins (70/30, 75/25) hold morning of surgery to up to 35% of morning dose or 50% of intermediate -acting component.
For insulin pump settings, the consensus is to continue the usual basal setting or follow the advice of the diabetes care provider. 1, 2, 4-6
During periods of stress as in the case of surgery and illness, the body releases stress hormones to maintain homeostasis: glucagon, epinephrine, growth hormone, and cortisol. These stress hormones individually contribute to increases in circulating glucose. For individuals on steroid supplementation therapy, the cortisol (produced by the adrenal gland) stress response may be suppressed.
It is common practice to prescribe stress steroids to patients on maintenance steroid therapy to prevent possible perioperative complications (most importantly refractory hypotension and shock) from adrenal hyporesponsiveness secondary to chronic adrenal suppression.
The origin of stress dose steroid usage appears to be historically based on case studies from the 1950s. There is sparse clinical evidence to support routine use of stress dose steroids and varying recommendation on dosing regimen of preoperative steroids for patients on maintenance steroid therapy.