DM is a condition with an absolute (Type 1) or a relative (Type 2) deficiency of insulin. Chapter 13 discusses the complex physiology of DM. Recent comprehensive reviews discuss perioperative glucose management.2,4,5 A fundamental concept is that the Type 1 diabetic patient has an absolute requirement for continuous exogenous insulin.1 In the absence of insulin, despite a normal or low blood sugar concentration, the patient with Type 1 DM will develop ketoacidosis. The pharmacokinetic profiles of the various insulin preparations warrant careful consideration (Table 60-1).6 Without a source of glucose in the perioperative period, a patient may develop hypoglycemia from the residual effects of a long-acting insulin preparation.
In the immediate perioperative period, it is generally recommended that patients receive regular insulin by intravenous (IV) bolus or IV infusion. The uptake of intramuscular or subcutaneous insulin may be unpredictable in the perioperative period because of changes in tissue perfusion.2,4,5
Patients with Type 2 DM can be managed with diet, an oral agent, insulin, or combinations of drugs including one of the newer medications (incretin mimetics, pramlintide). The pharmacokinetic and pharmacodynamic profiles of oral hypoglycemic agents differ markedly (Table 60-2). Some oral agents (eg, sulfonylureas) remain active for 24 hours, predisposing the patient to hypoglycemia during fasting. Other oral agents act as insulin sensitizers, improving the postreceptor action of insulin. Insulin sensitizers and incretin mimetics do not cause hypoglycemia when used in single-agent therapy. Some of these agents are newly introduced into clinical practice,7,8,9 so experience with their use in surgical patients during the perioperative period is limited. Clinicians may soon encounter patients treated with bromocriptine, an old drug with a good safety profile. The metabolic control is likely achieved by a central mechanism, possibly in the hypothalamus.10
Although both major types of DM can share a number of clinical features, such as the presence of neuropathy, peripheral vascular, cardiovascular, and renal disease, and a predisposition to infection (see Chapter 13), an appreciation of the essential and distinctive features of each type is important.
The patient with Type 1 DM usually is first diagnosed at a young age, but the disease may occur at any stage of life. Obesity is not a predisposing factor for Type 1 DM, unlike Type 2 DM. Conventional teaching holds that the patient with Type 1 DM is generally thin or of normal body habitus, but obesity may be present as a comorbid condition. The patient with Type 1 DM has an absolute requirement for chronic insulin therapy to prevent diabetic ketoacidosis (DKA). As a general rule, patients with Type 1 DM are sensitive to the effects of insulin compared to patients with Type 2 DM, and therefore receive relatively small doses of insulin to both control blood sugar levels and prevent DKA. Acute medical or surgical conditions can precipitate DKA (diagnostic criteria are listed in Table 60-3). Consequently, these patients may arrive urgently in the operating room and require surgical intervention (ie, due to trauma, acute abdomen, abscess, ischemic limb, coronary artery bypass grafting [CABG]) but may have a concurrent metabolic derangement. Therefore, intraoperative anesthetic management of the patient with Type 1 DM may include treatment of DKA.
Table 60-3 Typical Laboratory Findings during DKA and HONK ||Download (.pdf)
Table 60-3 Typical Laboratory Findings during DKA and HONK
|Serum glucose (mg/dL)||>300||>600||>600|
|Serum bicarbonate (mEq/L)||<15||≥15||<15|
|Serum osmolarity (mOsm/L)||≤320||>320||>320|
Features of DKA (Table 60-3) include circulatory depression, as acidosis and metabolic derangements can reduce cardiac contractility and peripheral vascular tone.11 Hyperglycemia with attendant hyperosmolarity produces osmotic diuresis, resulting in hypovolemia. Abnormalities often include hyperglycemia (although glucose usually is <500 mg/dL), intracellular dehydration, hyperkalemia, and hyponatremia. Dehydration frequently is severe because of poor oral intake due to the primary illness and is exacerbated by hyperglycemia-induced osmotic diuresis. Plasma potassium (K+) levels can be elevated because metabolic acidosis drives K+ from the intracellular space to extracellular fluids. Insulin concentrations are insufficient to maintain intracellular K+ levels, so total body K+ actually is depressed (reduced by 3-10 mEq per kilogram body weight). Measured sodium (Na+) concentrations are artificially lowered approximately 1.6 mEq/L for every 100 mg/dL that the glucose level is elevated above 100 mg/dL. Thus the serum Na+ level of a severely hyperglycemic patient may not reliably reflect the degree of dehydration. Plasma hypophosphatemia and hypomagnesemia commonly result from excessive urinary losses in DKA.
Management of DKA includes repletion of intravascular volume with electrolytes and water to resolve fluid deficits and help restore blood pressure, tissue perfusion, and glomerular filtration. Initial volume resuscitation usually is accomplished with normal saline even in the setting of hypernatremia. Vigorous hydration also decreases glucose levels by 20% to 40%. Insulin therapy (regular insulin by IV bolus and subsequent infusion) is crucial in treating DKA. Insulin inhibits gluconeogenesis and ketone production in the liver, and decreases lipolysis in adipose tissues. Insulin administration must be continued if acidosis or ketosis persists, even though glucose levels have normalized. During administration of insulin when plasma glucose concentrations decrease to less than 250 mg/dL, an infusion containing 5% dextrose (eg, D5NS, 100 mL/h) will prevent hypoglycemia. Blood glucose levels should be monitored every hour, with frequent electrolyte determinations.
Potassium and phosphate replenishment are essential for insulin's action. These electrolytes should be replaced carefully, after first verifying that the patient has normal renal function and adequate urine output. Ensure proper function of the IV access as extravasation of potassium can cause tissue damage. Rapid potassium administration can precipitate dysrhythmias. Potassium can be replaced with an equal mixture of potassium chloride and potassium phosphate.
- Serum K+ <3 mEq/L, give K+, 40 mEq/h
- Serum K+ <4 mEq/L, give K+, 30 mEq/h
- Serum K+ <5 mEq/L, give K+, 20 mEq/h
- Serum K+ ≥5 mEq/L, no replacement
Consideration should be given to bicarbonate therapy only for severe acidosis (eg, when arterial pH falls to <7.0) or hemodynamic instability, or for patients with cardiac rhythm disturbances. Following administration of bicarbonate, arterial pH levels should be monitored.
An emerging form of diabetes associated with obesity and presenting with ketoacidosis is called Flatbush Type 2 DM. Most or almost all of these patients can be treated with oral agents after initial management with intensive insulin therapy. Initial treatment of ketoacidosis in the patient with Flatbush Type 2 DM is the same as for the typical Type 1 DM patient.
Patients with Type 2 DM generally are older, obese, and subject to metabolic syndrome, a complex pathophysiologic state characterized by hypercholesterolemia, hypertriglyceridemia, hyperglycemia, hypertension, and Type 2 DM.12-14 In patients with metabolic syndrome, the cardiovascular risk of anesthesia and surgery may elevate markedly. Hypercoagulability is 1 feature of metabolic syndrome potentially relevant to these patients, who may be prone to thrombosis as a result of their surgical conditions or the consequences of surgery and anesthesia.15 Of burgeoning clinical importance is the growing population of young, typically obese, patients with Type 2 DM. The practitioner encounters a juvenile or adolescent patient with the combined anesthetic management challenges of youth, obesity, and diabetes. Type 2 DM may occur in young, nonobese adolescents (maturity-onset diabetes of the young [MODY]) because of autosomal dominant inheritance of a mutation in the glucokinase gene that results in impaired hepatic glucose uptake and reduced insulin secretion.
A fundamental concept of Type 2 DM is that patients with the condition usually produce sufficient insulin to avoid DKA, the severe metabolic consequence of absolute insulin deficiency seen in patients with Type 1 DM. However, patients with Type 2 DM have reduced cellular responses when insulin binds to its receptor. Patients are described as being resistant to the hypoglycemic actions of insulin. To achieve normal glucose levels, patients with Type 2 DM may require doses of insulin that are large compared to doses required for Type 1 DM therapy.
Initial medical therapy in the ambulatory Type 2 DM patient includes administration of agents to increase endogenous insulin release, reduce intestinal uptake of carbohydrates, or increase peripheral sensitivity to insulin. When these measures are insufficient to normalize blood sugars, insulin therapy should be initiated, but patients may require very high insulin doses. New classes of therapeutic agents, currently represented by pramlintide and agents acting along the incretin pathway, increase insulin secretion, reduce postprandial glucagon secretion, and suppress hepatic glucose production.8,8a,16
Hyperglycemic Hyperosmolar Nonketotic Coma
Hyperglycemic hyperosmolar nonketotic coma (HONK), also known as hyperglycemic hyperosmolar syndrome, is a clinical syndrome encountered in some Type 2 diabetic patients with decompensated DM.11 Features include hyperglycemia, hyperosmolarity, and dehydration (typical water deficit 10-12 L). Severe ketosis is rare, but mild acidemia can be caused by starvation ketosis, inadequate circulation, and lactic acidosis (Table 60-3). The precipitating factors for HONK are similar to those of DKA (Table 60-4). Patients presenting for surgery, especially urgent procedures, may have HONK as a comorbid condition requiring management during administration of their anesthetics. The classic presentation of patients with HONK includes fatigue, blurred vision, polydipsia, polyuria, leg cramps, and weight loss. The laboratory findings of HONK are related to dehydration and hypovolemia. Derangements in serum electrolyte levels occur, and hemoconcentration causes increases in blood levels of hemoglobin, protein, calcium, amylase, lactate dehydrogenase, and transaminases. Some patients present a mixed picture, with features of both DKA and HONK (Table 60-3).
Table 60-4 Precipitating Factors for Hyperglycemic Hyperosmolar Nonketotic Coma ||Download (.pdf)
Table 60-4 Precipitating Factors for Hyperglycemic Hyperosmolar Nonketotic Coma
|Precipitating Events||Pharmacologic Agents|
|Infection (pneumonia, urinary tract infection, sepsis)|
|Noncompliance with insulin regimen||β-Agonists||Protease inhibitors|
|First presentation of diabetes mellitus||Diuretics||Salicylates|
Impaired renal function
Fluid administration in the setting of HONK is crucial. The rate of fluid administration depends on the patient's volume status, total body water deficit, serum osmolarity, and renal and cardiac function. Normal saline (2-3 L) is an appropriate fluid bolus in a patient with adequate cardiac and renal function, and serum osmolarity less than 320 mOsm/L. Even larger fluid boluses may be required if serum osmolarity is greater than 320 mOsm/L. In hypotensive patients who do not respond to aggressive crystalloid administration, colloidal or vasopressor infusions are additional treatments. Central venous pressure or pulmonary arterial monitoring may help guide therapy, especially in patients with HONK who are elderly and at significant risk for concomitant cardiovascular disease.
Medical therapy for HONK includes a low-dose, continuous IV infusion of insulin. If no decrease in glucose levels occurs over the first 2 to 4 hours, doubling the insulin infusion rate every hour until a response occurs is recommended. Potassium chloride usually is administered as part of the fluid regimen. The total body potassium deficits encountered in HONK are modest compared to DKA because of the absence of acidosis (see guidelines for potassium replacement in DKA). Potassium acetate and/or potassium phosphate can be used in order to avoid excessive chloride levels. Bicarbonate need not be given unless lactic acidosis causes arterial pH to decrease to less than 7.0. Thrombotic/embolic events are common complications of HONK. Prophylaxis against thrombosis warrants consideration. Should thrombosis occur, an anticoagulating dose of IV heparin or low-molecular-weight heparin anticoagulation is indicated.
Perioperative Insulin/Glucose Management
As a rule, long-acting oral hypoglycemic agents (sulfonylurea drugs) should not be given before surgery to reduce the risk of hypoglycemia, signs and symptoms of which may be masked by general anesthesia. It is unlikely that insulin sensitizers will produce hypoglycemia. Theoretically, inhibitors of glucagon secretion (eg, GLP-1 analogues) may lead to hypoglycemia in the fasting state. However, the actions of these drugs are glucose dependent; they should have no effects when blood sugars are low. Nevertheless, prudence suggests that agents acting along the incretin pathway and pramlintide should be held on the day of surgery. Patients with Type 2 DM treated with insulin are at risk for hyperglycemia if their insulin is withheld completely. Typically, these patients receive about half of their usual morning insulin dose in the form of long-acting insulin preparations, such as NPH insulin. Short-acting insulins are omitted. Patients with Type 1 DM must receive some insulin. In this population, half of the usual morning dose of long-acting insulin may be appropriate before surgery. One key to management is frequent monitoring of glucose levels in all patients with DM. As a general rule, diabetic patients should undergo their anesthetic and surgical procedures as early in the day as possible. This limits the perturbations caused by prolonged fasting and disruption of customary diabetes medical regimens.
Recently, more patients have been managed with their insulin requirements supplied by continuous and bolus infusions delivered by an insulin pump. Recommendations for the perioperative period for patients with pumps include (1) maintaining the basal infusion rate of insulin, (2) omitting any preprandial insulin boluses in the fasting patient, (3) monitoring of glucose levels at frequent intervals, and (4) resuming the usual diet and insulin therapy regimen as soon as possible.16 However, the anesthesiologist must recognize that these pumps deliver the insulin dose subcutaneously. Uptake of the drug from this depot may be affected by alterations (usually reductions) in tissue perfusion that are commonly encountered during surgery or the perioperative period.3 Consequently, depending on the surgical circumstances, it may be advantageous to interrupt the continuous subcutaneous administration of insulin by pump and to substitute carefully titrated IV infusions of insulin. To decide on the initial IV insulin infusion rate, first determine the total 24-hour basal insulin dose typically administered by the subcutaneous infusion. Divide this basal dose by 24. Start the IV infusion with this number of units of regular insulin per hour, again with close monitoring of blood glucose and serum potassium levels.
Intraoperative Insulin Therapy
A variety of regimens exist for IV infusion of regular insulin in the operating room. For the routine surgical population, the "Vellore regimen" has been evaluated.18 Other schemes also are acceptable2,19 as long as glucose and potassium levels are closely monitored and treated when necessary. Table 60-5 outlines 1 practical method of insulin administration in the operating room that is used at our institutions. Cardiac surgical patients20 and pediatric surgical patients11 may benefit from regimens tailored to the special needs of these particular populations.
Table 60-5 A Perioperative Intravenous Regular Insulin Regimen ||Download (.pdf)
Table 60-5 A Perioperative Intravenous Regular Insulin Regimen
A. Initial regular insulin IV bolus: 0.05-0.1 U/kg
Dose additional boluses based on glucose levels.
B. Regular insulin infusions (1 U regular insulin/mL normal saline)
Initial Regular Insulin Infusion Rate (U/h)
| Type 1 DM (female)||0.5|
| Type 1 DM (male)||1.0|
| Type 2 DM (male or female)||1.0|
Notes on IV Regular Insulin Action
1. Onset is immediate.
2. Duration is ˜1 h.
3. Duration of action is prolonged in renal insufficiency.
Adjustment of IV Regular Insulin Infusion Rate (U/h) based on hourly point of care glucose measurement
|Glucose (mg/dL)||Rate Change||Other Rx|
|<70||Hold 30 min||Give D50, 15-20 mL. Recheck blood glucose level after 30 min. Give more dextrose until blood glucose level >70 mg/dL.|
|70-120||↓ 0.3 U/h|
|181-240||↑ 0.3 U/h|
|241-300||↑ 0.6 U/h|
|>300||↑ 1.0 U/h|
Notes on IV Regular Insulin Dosing
1. Insulin guidelines assume patient is fasting and is not in diabetic ketoacidosis.
2. Dosing must be individually titrated based on frequent blood glucose monitoring.
Perioperative Glucose Target Range
Several studies providing evidence for the clinical benefits of tight glucose control (eg, 80-110 mg/dL) in critically ill patients led to initially enthusiastic adoption of intensive insulin therapy (IIT) regimens. Later reports demonstrated adverse (eg, hypoglycemia) or neutral effects of IIT. Current expert opinion suggests keeping glucose below 180 mg/dL in the critically ill patient.3,4,22-24 Few data exist to guide intraoperative glucose management practices. In some surgical situations (eg, neurovascular procedures or carotid endarterectomy) associated with significant risk for cerebral ischemia, it might be argued that blood glucose levels should be more tightly controlled to avoid hyperglycemia. For other procedures, the optimum insulin regimen and the ideal range of blood glucose levels for routine anesthetics remain undetermined.23,25,26
Glucose monitoring is the foundation for safe and effective glucose management and perioperative insulin therapy. Clinicians use point-of-care testing with various devices or send arterial or venous blood samples to a central laboratory for analysis.3,4 The technology for glucose analysis is complex.27 Unrecognized pitfalls exist with the convenient handheld devices, and clinicians must recognize that multiple factors have an impact on the accuracy of the result, upon which therapeutic decisions may be based.28 Potential confounding factors include anemia, hypoxemia, hyperoxia, the presence of other sugars, elevated triglyceride, bilirubin, urea or uric acid levels, and perhaps also blood pH and body temperature.
Metformin is an oral hypoglycemic agent of the biguanide class with an important role in Type 2 diabetes therapy, particularly because of its favorable effects on cardiovascular mortality.29 This drug, which has multiple pharmacologic effects, has also been associated with the serious side effect of lactic acidosis, which may become life threatening. Whether metformin causes lactic acidosis or exacerbates lactic acidosis resulting from other conditions remains undetermined.30,31, When administered according to guidelines and avoiding contraindications including renal and hepatic insufficiency and a history of alcohol abuse, the incidence of lactic acidosis is very low.29 In conditions where tissue hypoxia already exists (including circulatory failure) or circulatory insufficiency is anticipated (eg, major surgery), it is prudent to withhold metformin. In anticipation of IV radiologic contrast exposure, metformin should be stopped and not restarted until the creatinine level has been checked to confirm baseline renal function. Recognizing that conclusive data do not exist to support their suggested guidelines, Jones et al32 and Vreven and De Kock33 proposed that metformin be withdrawn 2 days before general anesthesia and reinstated when renal function is demonstrated to be stable. This is not universally practiced. Metformin should not produce hypoglycemia in the fasting preoperative patient.
Steroid (Glucocorticoid) Therapy: Implications for DM
Administration of pharmacologic doses of glucocorticoids increases resistance to insulin action by inhibiting glucose uptake into muscle and fat.34 In many patients the effect is primarily postprandial hyperglycemia. Thus morning fasting glucose levels are only mildly elevated, but glucose levels rise substantially after meals in the afternoon and evening.
Glucose levels will increase in patients with known diabetes. Glucocorticoid therapy reveals previously undiagnosed insulin resistance in 25% of all patients receiving such treatment.18 The hyperglycemia resulting from glucocorticoid therapy can be managed with insulin, oral hypoglycemic agents, or combination therapy. When glucocorticoid therapy is tapered, insulin resistance decreases with a lag of 1 to 3 days. Hyperglycemia therapies (eg, insulin infusions) must then be reduced to avoid hypoglycemia. The complexities of the patient's regimen for controlling hyperglycemia must be considered when managing medications and glucose in the perioperative period.
Postoperative stress usually leads to excess endogenous glucocorticoid production and consequent insulin resistance. This may result in hyperglycemia lasting 1 to 3 days after the procedure or for as long as significant infection or pain-related stress is present. Treatment of this manifestation of hyperglycemia is accomplished by administering a long-acting insulin plus a short-acting insulin at mealtime in the patient who is able to eat. Other patients may require regular insulin administered by IV infusion.
Alpha cells of the pancreatic islet secrete glucagon. Glucose is the most important regulator of glucagon secretion. Hyperglycemia decreases glucagon secretion. Hypoglycemia stimulates glucagon secretion via direct effects on islets and via central nervous system pathways activated by hypoglycemia. β-Adrenergic receptor activation stimulates glucagon secretion.36 Glucagon acts primarily on the liver to increase both glycogenolysis and gluconeogenesis. Increased glucose output balances glucose utilization during the fasting state to maintain euglycemia.37 Patients with hepatic or pancreatic insufficiency are theoretically at risk for hypoglycemia as a result of lack of glucagon effects. In addition, β-blocker therapy potentially reduces glucagon secretion, thereby potentially increasing the risk of hypoglycemia. The implication for anesthetic management is the need to monitor glucose levels frequently in patients at risk and to intervene as needed.
Epinephrine and glucagon are the most important hormones maintaining euglycemia during the fasting state.38 The central nervous system reacts to hypoglycemia by stimulating the secretion of epinephrine. Activation of pancreatic α-adrenergic receptors by epinephrine inhibits insulin secretion. β-Adrenergic receptor activation stimulates the secretion of glucagon. Epinephrine, via β2-adrenergic receptors, also acts directly on the liver to increase glycogenolysis and gluconeogenesis. Therefore, patients at risk for blunted sympathetic responses, either following neuraxial anesthesia or from receiving β-blocker therapy, may fail to react normally to hypoglycemia. The implication for anesthetic management is, again, a need to anticipate potential hypoglycemia, with close monitoring of glucose levels in patients at risk, and to treat as needed.
Glucocorticoids and Growth Hormone
Growth hormone (GH) and cortisol play minor roles in the restoration of euglycemia after hypoglycemia. The prevention of cortisol secretion and GH deficiency does not inhibit restoration of euglycemia after hypoglycemia.39 The hyperglycemic response to the combination of glucagon, epinephrine, and cortisol is larger than the response to each of these hormones given individually, suggesting that synergism contributes to normal physiologic responses to hypoglycemia.40
Some patients with long-standing DM and frequent bouts of hypoglycemia lose their normal sympathetic response to low blood sugar levels. The failure to consciously recognize low blood sugar levels is known as "hypoglycemic unawareness." Fasting in the perioperative period, particularly in the setting of continued insulin therapy administered by infusion pump, may predispose these patients to potentially dangerous hypoglycemia. The anesthesiologist cannot rely on such patients to symptomatically monitor their own blood glucose levels and to respond appropriately, even when managed with regional anesthesia and minimal sedation. Blood glucose measurement, and appropriate therapy, is essential for these patients.
DM: Implications for Anesthesia
Although general anesthesia may be mandatory for some surgical procedures, other options (including regional anesthesia or neuraxial anesthesia) exist for some situations.41 Neuraxial anesthesia may provide an advantage by blocking "stress responses" to surgery involving counterregulatory hormones such as epinephrine and glucocorticoids. Regional or neuraxial block anesthetic techniques may allow some diabetic patients to return to their customary diets earlier than they would if given general anesthesia, facilitating resumption of chronic diabetes regimens. Metabolic control in the diabetic patient may be improved by regional anesthetic techniques, at least in some patient populations.42 Regional anesthesia or neuraxial techniques may also be useful for patients with diabetic gastroparesis who are at elevated risk for aspiration under general anesthesia, or who may be difficult to intubate because of stiff joints (including the temporomandibular joints and the cervical spine) associated with their disease. In addition, preexisting autonomic neuropathy may compound the effects of sympathectomy produced by neuraxial block. Data suggest that cerebrospinal fluid (CSF) composition differs between patients with DM and healthy patients, and that this difference correlates with enhanced sensitivity to neuraxial drugs.43
There is some concern that patients at risk for diabetic neuropathy may be more likely to develop peripheral nerve injury in association with regional or neuraxial techniques, either from local anesthetic toxicity or mechanical trauma from the block needle.44 Only a small amount of published evidence addresses these issues. Blumenthal et al describes 1 patient with a preexisting, nondiabetic, asymptomatic polyneuropathy who developed symptomatic neuropathy after a peripheral nerve block.45 Hebl et al reported 2 patients in a retrospective series who developed exacerbations of preexisting neuropathy after neuraxial anesthesia or analgesia. Both patients had Type 2 DM.46 These authors suggest that local anesthesia toxicity is a possibility. Adjuvants (eg, clonidine) may prove beneficial in providing desired anesthetic effects with smaller doses of local anesthetics, thereby reducing toxicity risks.47 McAnulty and Hall48 conclude that there is no evidence to indicate that regional anesthesia alters overall surgical morbidity and mortality in the diabetic patient population. Consequently, a well-conducted anesthetic, regardless of specific technique, probably is the most important factor in the care of the diabetic patient. Of note, general anesthesia often masks the autonomic response to hypoglycemia, and changes in vital signs can easily be misinterpreted as a response to increased surgical stimulation rather than hypoglycemia. Consequently, close monitoring of glucose levels in patients at risk for hypoglycemia and appropriate therapy are essential.
Specific Surgical Procedures and Glucose Homeostasis
Total pancreatectomy eliminates insulin-producing islet cells as well as cells secreting the counterregulatory hormone glucagon. This surgery renders the patient a Type 1 diabetic with an absolute requirement for insulin therapy. The biologic effect of insulin molecules bound to cellular receptors lasts for approximately 1 hour, but the chemical half-life of insulin in the circulation is just a few minutes. Consequently, following a total pancreatectomy, the need for insulin therapy to prevent DKA begins within 60 minutes of devascularizing the pancreatic islets.
Surgery for insulinoma or glucagonoma poses particular management challenges. Glucagonoma may cause elevations in glucose and resistance to insulin during surgery, so glucose levels should be monitored closely and managed as needed. Insulinomas may cause life-threatening, profound hypoglycemia. There can be wide swings of glucose levels perioperatively. Frequent measurements of glucose and therapeutic interventions (IV insulin or IV glucose administration) may be necessary.