Diabetes Mellitus

Description

Diabetes mellitus (DM) has been increasing in the last several decades, likely due to its strong association with obesity.
DM is one of the leading causes of morbidity and mortality in the US population, with an economic cost of $171 billion annually.

Epidemiology

Incidence

In the US: 1.3 million new cases annually

Prevalence

In the US: 25.8 million people have the disease, accounting for 8.3% of the population.

Morbidity

A risk factor for perioperative surgical and anesthetic complications

Mortality

7th leading cause of death in the US

Etiology/Risk Factors

Type I diabetes risk factors:
- Genetics and family history
- Infection or illness of the pancreas
Type II diabetes risk factors:
- Obesity or overweight
- Impaired glucose tolerance
- Insulin resistance
- Hypertension
- History of gestational diabetes
- Sedentary lifestyle
- Family history
- Polycystic ovary syndrome
- Age
- Ethnic background: Diabetes occurs more often in African Americans, Hispanic Americans, Native Americans, Asian Americans, and Pacific Islanders.

Physiology/Pathophysiology

Normally, blood glucose is tightly regulated by:
- The hormonal system which consists of a balance between the hypoglycemic insulin and hyperglycemic counter-regulatory hormones such as glucagon, epinephrine, and cortisol.
- Neural mechanisms; glucose sensors in various organs are capable of sending messages.
- Together, these systems modulate carbohydrate metabolism by controlling endogenous production and entrance of glucose into the cells.
Type I diabetes is caused by the complete lack of insulin secretion from the pancreas. The inability of cells to take in glucose leads to metabolic abnormalities, including hyperglycemia, lipolysis, proteolysis, and ketogenesis.
Type II diabetes is caused by insulin deficiency or insulin resistance and can result in dehydration and a hyperosmolar state. Type II diabetes patients are usually ketosis-resistant since their insulin concentration in the circulation is sufficient to prevent ketogenesis.

Anesthetic Goals/Guiding Principles

Preoperative fasting, long-acting insulin or oral antihyperglycemics, and surgical stress can result in episodes of hypoglycemia or hyperglycemia. Perioperative glucose testing and treatment should be performed, as appropriate.
Microvascular and macrovascular disease can result in end-organ damage; preoperative evaluation should assess the involvement and severity. Maintain hemodynamic stability to avoid hypoperfusion to the heart, brain, and kidneys.
Consider the possibility of gastroparesis and pulmonary aspiration; if high risk, modify NPO guidelines, premedicate to decrease gastric volume and acidity, and place a cuffed endotracheal tube.

Diagnosis ⬆ ⬇

Symptoms

Polyuria, polydipsia, and polyphagia are associated with hyperglycemia and can suggest new-onset diabetes.
Autonomic neuropathy is associated with perioperative hypotension and may be suggested by dizziness and syncope. Impotence is a sign of autonomic nervous dysfunction.
Decrease in vision associated with diabetic retinopathy

History

Assess metabolic control: Daily glucose level/range, usual dietary intake, physical activity, hemoglobin A1C level, episodes of hypoglycemia or ketoacidosis, and medications.
Assess the severity of concomitant organ dysfunction and optimize as appropriate. A prior myocardial infarction is a clinical predictor for perioperative cardiac events. Hypertension should be checked and controlled prior to surgery.
Gastroparesis manifests as indigestion, nausea, vomiting, diarrhea, and abdominal distension.

Signs/Physical Exam

Usually nonspecific
Abnormal physical exams are usually related to the complications associated with diabetes.
"Stiff joint syndrome": Limited joint mobility may be associated with a potentially difficult tracheal intubation.
Orthostatic hypotension or resting tachycardia associated with autonomic neuropathy

Medications

Exogenous insulin: The types of insulin include rapid-acting (Humalog, Novolog, Apidra), short-acting (Regular, Velosulin), intermediate-acting (NPH, Lente), long-acting (Ultralente, Lantus, Levemir), and pre-mixed (Humulin 70/30, Novolin 70/30, Novolog 70/30, Humulin 55/50, Humalog 75/25).
Oral agents: Sulfonylureas stimulate the pancreas to release more insulin (glipizide, glyburide, glimepiride). Biguanides improve the ability of insulin to move glucose intracellularly (metformin). Thiazolidinediones improve the effectiveness of insulin (pioglitazone, rosiglitazone). Alpha-glucosidase inhibitors block enzymes that digest starch; they slow the rise in blood glucose (acarbose, miglitol). Meglitinides stimulate the pancreas to release more insulin (repaglinide, nateglinide). Dipeptidyl peptidase IV inhibitors increase insulin secretion from the pancreas and decrease glucose production from the liver (sitagliptin, saxagliptin). Combination therapy combines the above-described mechanisms for improved glycemic control (glyburide/metformin; glipizide/metformin; rosiglitazone/metformin).
ACE inhibitors or angiotensin receptor antagonists provide protective effects in diabetes patients with CHF and renal insufficiency in addition to the treatment of hypertension. May be associated with refractory hypotension.

Diagnostic Tests & Interpretation

Labs/Studies

Labs: Glucose, HgA1C, BUN/Cr (renal function), electrolytes
EKG: Silent ischemia or old infarcts
Cardiac stress tests if indicated

CONCOMITANT ORGAN DYSFUNCTION

Neurologic: Cerebrovascular disease (stroke); peripheral neuropathy from direct mesangial expansion and injury from chronic hyperglycemia
Retinopathy is present in 28.5% of patients aged 40 years; it is the leading cause of new cases of blindness in adults aged 20–74 years.
Cardiovascular: Heart disease (comprises 68% of patients 65 years who died from diabetes-related complications). Mechanisms are complex and multifactorial and are related to both macrovascular and microvascular dysfunction. Hypertension (67% of diabetics); progression is likely due to activation of the local renin–angiotensin system.
Renal: Leading cause of renal failure (microvascular disease)
Metabolic: Diabetic ketoacidosis (DKA) is the most serious acute metabolic emergency. Hypoglycemia is more common than DKA in IDDM and is dangerous.

Circumstances to delay/Conditions

Severe hypoglycemia or hyperglycemia, especially in patients with symptoms of ketoacidosis or hyperosmolar nonketotic coma
Acute infections
Severe dehydration or electrolyte imbalance

Classifications

Type I diabetes (insulin-dependent) is caused by absolute insulin deficiency secondary to immune-mediated or idiopathic causes. Patients are also prone to ketosis.
Type II diabetes (non-insulin dependent) is usually adult onset and secondary to relative insulin deficiency and resistance.

Treatment ⬆ ⬇

PREOPERATIVE PREPARATION

Premedications

Oral agents should be withheld on the morning of surgery to avoid perioperative hypoglycemia. Metformin should be withheld for 24 hours; it has been associated with fatal metabolic acidosis.
Night doses of long acting insulin and morning doses are often decreased (or withheld) to avoid hypoglycemia in the fasting patient.
Glucose level should be checked.

INTRAOPERATIVE CARE

Choice of Anesthesia

Depends on the type and duration of surgery, comorbidities, and patient's preference
Regional anesthesia (spinal, epidural, or peripheral nerve blocks) may modulate the secretion of insulin and catabolic hormones and block the body's response to surgical stress under general anesthesia. However, it may increase risks of profound hypotension (especially in patients with autonomic neuropathy), infection, and vascular injury. There is some evidence to suggest that local anesthetics are more toxic to peripheral nerves in diabetics, and the standard nerve stimulator utilized for localization may exhibit reduced effectiveness.

Monitors

Standard ASA monitors
Invasive BP (in patients with severe CAD, autonomic neuropathy, and for close monitoring of glucose during prolonged surgery under general anesthesia)

Induction/Airway Management

Consider the possibility of a difficult airway in patients with stiff joint syndrome.
Intravenous induction should be accomplished by careful titration to avoid hypotension.
- Benzodiazepines and etomidate may decrease ACTH secretion and block adrenal steroidogenesis, respectively; this can decrease cortisol synthesis.
- Propofol may cause profound hypotension in patients with severe autonomic neuropathy.
Rapid-sequence induction with cricoid pressure should be considered in patients with gastroparesis to decrease the risk for pulmonary aspiration.

Maintenance

for general anesthesia, a "balanced technique" (combination of volatile agents, narcotics, and intravenous anesthetics) is preferable to reduce the potential metabolic disturbance from each individual agent. Volatile agents may impair the insulin response to elevated glucose from the sympathetic stimulation of surgery and general anesthesia.
Total intravenous anesthesia with propofol may result in hypotension. Additionally, there may be a decreased ability to metabolize propofol because of the impaired lipid metabolism in diabetic patients.
Narcotics may have the benefit of hemodynamic stability, as well as stable metabolic and hormonal stages.
Glucose control: Intraoperative monitoring and treatment with IV insulin (or dextrose) should be considered, particularly in brittle diabetics (q 30–60 minutes, with intraoperative insulin either via IV bolus or infusion). Continuous intravascular glucose monitors may aid in tight blood glucose control perioperatively and in critically ill patients. Currently, they are not in common use.
Maintain normothermia; hypothermia can worsen postoperative insulin resistance.

Extubation/Emergence

Ensure that patients have fully recovered from muscle relaxants or been adequately reversed. Patients should be awake with intact protective gag reflexes prior to extubation.
Prophylaxis for postoperative nausea and vomiting. Metoclopramide may decrease postoperative nausea and vomiting (PONV) by enhancing gastric emptying, especially in patients with gastroparesis.

Follow-Up ⬆ ⬇

Bed Acuity

Vigilant monitoring to detect and treat hypotension, myocardial ischemia, and acute renal failure
In certain circumstances (brittle, high-risk surgery) hourly glucose monitoring (and treatment) may be appropriate.
Close monitoring for respiratory dysfunction, hypothermia, and hypoxia
Avoid oversedation that may delay the identification of mental alteration from hypoglycemia or ketoacidosis

Complications

Metabolic abnormality (hypoglycemia, hyperglycemia, lactic acidosis)
Myocardial infarction
Perioperative aspiration
Acute renal failure
Infection

References ⬆ ⬇

American Diabetes Association . Diabetes statistics. 2011.
Lena D , Kalfon P , Preiser JC , et al. Glycemic control in the intensive care unit and during the postoperative period. Anesthesiology. 2001;114(2):438–444.
McAnulty GR , Robertshaw HJ , Hall GM. Anesthestic management of patients with diabetes mellitus. Br J Anaesth. 2000;85(1):80–90.
Rigaud M , Filip P , Lirk P , et al. Guidance of block needle insertion by electrical nerve stimulation: A pilot study of the resulting distribution of injected solution in dogs. Anesthesiology. 2008;109:473–478.
Schricker T , Wykes L , Carli F. Epidural blockade improves substrate utilization after surgery. Am J Physiol. 2000;279:E646–E653.
Skjaervold NK , Solligard E , Hjelme DR , et al. Continuous measurement of blood glucose: Validation of a new intravascular sensor. Anesthesiology. 2011;114(1):120–125.

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Basics ⬇