I. INTRODUCTION

A. Recognition of endocrine disorders requires a high index of suspicion among clinicians in the postoperative period. The effects of anesthesia often mask initial symptoms of endocrine abnormalities in the postoperative anesthesia care unit (PACU), necessitating vigilance upon the part of caregivers to initiate early treatment and prevent complications. Ideally, a comprehensive preoperative evaluation of patients alerts clinicians to preexisting endocrine disease and lowers the risk of postoperative adverse events.

II. GLUCOSE CONTROL

A. Effects of Surgery on Blood Glucose Levels

1. General anesthesia and surgery trigger a neuroendocrine stress response, with release of epinephrine, glucagon, cortisol, growth hormone, and inflammatory cytokines into the systemic circulation. These hormones function to increase insulin resistance, decrease peripheral glucose utilization, decrease insulin secretion, and increase lipolysis and protein catabolism, ultimately creating a hyperglycemic state. The degree of this hyperglycemia varies between patients and depends upon the type of anesthesia, preoperative comorbidities, and the extent and type of surgery. General anesthesia, for example, disrupts metabolism to a greater extent than epidural anesthesia. Disruption of caloric intake prior to and during surgery also alters the normal hyperglycemic response. Such factors impede prediction of final glycemic balance in the postoperative period.

2. Hyperglycemia

a. Definition: >200 mg/dL in the postoperative area.

1. associated with increased risk of stroke, congestive heart failure, and morbidity/mortality

2. associated with increased surgical site infections

3. associated with cardiac cell death and reduced coronary collateral blood flow by triggering an exaggerated ischemia-reperfusion cellular injury

4. triggers platelet hyperactivity, increasing thrombosis. This results in increased levels of interleukin-6, interleukin-8, and tumor necrosis factor-α, creating a pro-inflammatory response.

5. leads to endothelial cell dysfunction, inactivation of nitric oxide, decreased synthesis of prostacyclin, and increased synthesis of endothelin 1, which all decrease local blood flow.

6. decreases renal tubular absorption capabilities, resulting in hypovolemia secondary to an osmotic diuresis

b. Maintain glycemic target <180 mg/dL for all surgical patients

1. More stringent protocols increase the risk of hypoglycemic events, resulting in increased mortality.

a. Intensive insulin therapy with target blood glucose of 80 to 110 mg/dL increases incidences of severe hypoglycemia and increases mortality when compared to the more permissive blood glucose ranges of 140 to 180 mg/dL (7.8 to 10 mmol/L) and 180 to 200 mg/dL (10 to 11.1 mmol/L).

2. General hospitalized population: Aim for fasting glucose of <140 mg/dL (7.8 mmol) and random glucose levels <180 mg/dL (10 mmol/L)

c. Maintain nutrition and electrolyte balance

B. Hypoglycemia

1. Definition: random glucose <40 mg/dL (2.2 mmol/L).

2. “Cut off value” is often debated, but PACU medical staff should be concerned with a level <70 mg/mL.

3. Causes: Most commonly long-acting insulin in patients with difficult to control diabetes

4. Potentially life-threatening: Underdiagnosed in the PACU setting due to sedation and anesthesia. If left untreated, can result in lethal cardiac arrhythmias and death.

a. Preoperative identification of patients prone to hypoglycemia significantly lowers risk.

1. High-risk patients: Past medical history of difficult to control diabetes requiring strict glucose monitoring, a history of uncontrolled glucose levels, or documented frequent hypoglycemic episodes

b. Preoperative titration of home diabetes regimen helps to avoid episodes of hypoglycemia in the postoperative setting

c. Regular measurement of glucose levels (point of care [POC]) postoperatively ensures prompt treatment of abnormalities

5. Postoperative clinical manifestations

a. Early recovery (Phase 1): Symptoms are usually nonspecific, and difficult to recognize. Frequently first detected by monitoring blood glucose levels upon arrive to PACU (in patients with known diabetes)

b. Late recovery (Phase 2): Recognition of the following symptoms:

1. tremor, palpitations, increased arousal, anxiety, sweating, and hunger

c. If left untreated, hypoglycemia can result in:

1. changes in level of consciousness, seizures, coma, and death

6. Treatment

a. Early recovery (Phase 1): sedated, anesthetized patient with blood glucose of <70 mg/dL

1. administer intravenous (IV) dextrose 25 g and repeat blood glucose test in 5 to 10 minutes

b. Late recovery (Phase 2): In an awake patient with an intact swallow and gag reflex

1. 15 g of carbohydrates (glucose tablet, sweetened fruit juice), recheck in 10 minutes or if symptoms resolve

c. Late recovery (Phase 2): patients unable to ingest by mouth

1. 25 g of 50% dextrose IV, recheck blood glucose in 5 to 10 minutes

III. DISORDERS OF GLUCOSE HOMEOSTASIS

A. Hyperglycemia

1. Causes

a. Stress hyperglycemia (Hyperglycemic Stress Syndrome)

1. transient elevations in blood glucose due to a catecholamine-induced stress response that occurs during acute illness, in patients with and without a history of diabetes mellitus (DM)

b. Medication-induced hyperglycemia

1. caused or aggravated by glucocorticoids, octreotide, vasopressors, and immunosuppressants, in patients with and without a history of DM

c. Dextrose-containing IV fluids administered in the perioperative phase

d. Excess counterregulatory hormones, as detailed above

e. Pancreatic disease with insufficient circulating insulin

f. Preoperative diabetes

2. Postoperative clinical manifestations

a. Early recovery (Phase 1): Unexplained diuresis, tachycardia, hypotension, anion gap metabolic acidosis, hyponatremia, and hyperkalemia.

b. Late recovery (Phase 2): Clinical signs and symptoms are vague, especially following administration of anesthetic agents. At baseline, one-third of patients with DM are asymptomatic. Most common symptoms include polyphagia, polydipsia, polyuria, confusion, and coma.

3. Treatment

a. Corrective insulin

1. Sliding scale for stable population

2. IV insulin infusion for critically ill population (Table 25.1)

B. Diabetic Ketoacidosis (DKA)

1. Precipitated from stress of surgery, or from the peri-operative use of mediations that alter metabolism. DKA is a medical emergency, requiring immediate recognition and intervention.

a. Triad of hyperglycemia, anion gap metabolic acidosis, and ketonemia. Serum glucose >800 mg/dL (44 mmol/L), predominately 350 to 500 mg/dL (19.4 to 27.8 mmol/L). Can exceed 900 mg/dL (50 mmol/L) in the presence of coma. Commonly evolves rapidly, over a 24-hour period.

b. Medications that can precipitate DKA include:

1. glucocorticoids, high-dose thiazide diuretics, sympathomimetic agents, and second-generation “atypical” antipsychotic agents

2. Postoperative clinical manifestations

a. Neurologic deterioration is seen at a plasma osmolality above 320 to 330 mOsmol/kg. Often are masked by effects of recent anesthesia.