Diabetes Mellitus in the Cardiac Care Unit



Diabetes Mellitus in the Cardiac Care Unit


Jeanine Albu

Greg Dodell

Aastha Pal

Edgar Argulian

Eyal Herzog



DIABETES MELLITUS: GENERAL PRINCIPLES


WHAT IS DIABETES MELLITUS? DIAGNOSIS AND CLASSIFICATION

The defining feature of diabetes mellitus is an inappropriate elevation of blood glucose—hyperglycemia. This could be because of excessive glucose production, impaired glucose clearance, or both. Sustained, chronic hyperglycemia, over several years, leads to tissue injury resulting in chronic micro- and macrovascular complications such as diabetic neuropathy, retinopathy, and nephropathy; and atherothrombotic vascular diseases. “Inappropriate” hyperglycemia has been defined by the experts as the level that, if chronically sustained, will lead to the development of diabetic complications.

The current criteria used to make the diagnosis of diabetes mellitus are listed in Table 32.1.1 According to the American Diabetes Association 2011 criteria, either random plasma glucose, fasting plasma glucose, an oral glucose tolerance test, or a hemoglobin A1C (% glycosylated hemoglobin, A1C) can be used to diagnose diabetes.1 and 2

Diabetes mellitus is currently classified by etiology as type 1, type 2, gestational, or other specified types (Table 32.2).1 Type 1 diabetes is characterized by absolute or severe insulin deficiency.3 Type 2 diabetes is a complex polygenic disease characterized by both insulin resistance and relative insulin deficiency, that is, insulin levels and secretion are inappropriate to the levels of insulin resistance and out of sync with the glucose stimuli (dual defect).4,5 Gestational diabetes mellitus (GDM) is characterized by onset during pregnancy owing to increased insulin resistance generated by the hormonal milieu. Typically, it resolves at the end of pregnancy; however, women with gestational diabetes are at high risk for developing type 2 diabetes later in life.6 Other specific types of diabetes listed by etiology are a result of genetic defects in β-cell function and/or insulin action (monogenic diabetes), exocrine pancreatic disease, some endocrinopathies, drug or chemically induced (exogenous corticosteroid administration, etc.), or other rare forms (infections, immune-mediated, etc.). These specific forms could manifest clinically in a similar fashion to either type 1 or type 2 diabetes.


Type 1 diabetes.

Certain clinical aspects of diabetes presentation are characteristic of type 1 diabetes: diabetic ketoacidosis; signs of insulin deficiency such as weight loss and/or blood glucose level >250 mg per dl accompanied by nonfasting positive urine ketones acute onset in a child or young adult triggered by recent infection or viral illness; onset during puberty or association with other autoimmune diseases (thyroiditis, Graves’ disease, pernicious anemia, celiac, and Addison disease).


Type 2 diabetes.

The pathogenesis of type 2 diabetes is very different from that of type 1 diabetes. As opposed to type 1 diabetes, in type 2 diabetes, insulin resistance is almost universally present, and the defect in insulin secretion is milder—the secretion is just not high enough to overcome the resistance (β-cell dysfunction). Type 2 diabetes is often preceded by a condition called prediabetes characterized either by abnormal fasting glucose levels (impaired fasting glucose or IFG) or by impaired glucose tolerance (IGT; abnormal postprandial glucose) that leads to increased levels of A1C (Table 32.1). During the prediabetes stage, there is a gradual increase in insulin resistance as a result of various causes (aging, obesity, physical inactivity, or genetics) and, when not accompanied by an increase in insulin secretion, will eventually result in elevated blood glucose levels in the diabetic range. Prediabetes can be identified through the same tests used to diagnose diabetes (Table 32.1). It is now recommended that individuals at risk be screened for the presence of type 2 diabetes (Table 32.3).1 During this screening, normal glucose tolerance, prediabetes, or full-blown diabetes can be identified. The screening is very important because (1) preventive measures such as weight loss and/or increased physical activity and sometimes pharmacologic measures could deflect the development of type 2 diabetes in the individuals with prediabetes; and (2) early diagnosis and treatment of the clinical manifestation of type 2 diabetes could prevent chronic complications and improve chances of survival.








TABLE 32.1 Diagnosis of Diabetes Mellitus








































CRITERIA FOR THE DIAGNOSIS OF DIABETES


1.

A1C ≥ 6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay (http://www.ngsp.org/prog/index.html, accessed 4/13/2010).*


OR


2.

FPG ≥ 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.*


OR


3.

Two-hour plasma glucose ≥200 mg/dl (11. 1 mmol/l) during an OGTT. The test should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75g anhydrous glucose dissolved in water.*


OR


4.

In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dl (11. 1 mmol/l).


* In the absence of unequivocal hyperglycemia, criteria 1-3 should be confirmed by repeat testing.


CATEGORIES OF INCREASED RISK FOR DIABETES (PRE-DIABETES)**


1.

FPG 100-125 mg/dl (5.6-6.9 mmol/l) [IFG]


2.

2-h PG in the 75-g OGTT 140-199 mg/dl (7.8-11.0 mmol/l [IGT]


3.

A1C 5.7-6.4%


** For all three tests, risk is continuous, extending below the lower limit of the range and becoming disproportionately greater at higher ends of the range.


Adapted from American Diabetes Association: clinical practice recommendations. Diabetes Care. 2011;34(suppl 1).










TABLE 32.2 Classification of Diabetes Mellitus



















TYPE 1 DIABETES




  • Immune Mediated



  • Idiopathic


TYPE 2 DIABETES




  • May range from predominately insulin resistant to predominantly insulin deficient


GESTATIONAL DIABETES


OTHER SPECIFIC TYPES




  • Genetic defects of β-cell function



  • Genetic defects in insulin action



  • Diseases of exocrine pancreas



  • Endocrinopathies



  • Drug- or chemical-induced diabetes



  • Infections



  • Uncommon forms of immune-mediated diabetes



  • Other genetic syndromes sometimes associated with diabetes


Adapted from Barker JM, Eisenbarth GS. Genetic counseling for autoimmune type 1 diabetes. In: Liebovitz HE, ed. Therapy for Diabetes Mellitus and Related Disorders. 5th ed. Alexandria, VA: American Diabetes Association and Library of Congress Publication; 2009.



Prediabetes.

It is also part of the metabolic syndrome, defined as a clustering of risk factors that predict the development of both type 2 diabetes and cardiovascular disease (CVD).7,8 More than 80% of patients with type 2 diabetes have metabolic syndrome and clustering of risk factors for CVD: hypertension, dyslipidemia, and associated inflammation and hypercoagulable state.7,8 The clustering of these risk factors predicts the development of CVD even independent of the degree of hyperglycemia. The treatment of the risk factors and the underlying pathophysiological causes could prevent both diabetes and CVD. The most prominent underlying modifiable pathophysiological causes are abdominal obesity and insulin resistance.9 Inflammation and hypercoagulable states are also important to address. The comprehensive treatment of the metabolic syndrome includes smoking cessation, assessment of diabetes risk and implementation of diabetes prevention strategies, control of blood pressure, control of glucose if type 2 diabetes is present, reduction of abdominal obesity, increase in physical activity to at least 30 minutes of activity daily (above usual), decrease in saturated fats to <7% of total calories, elimination of trans fat, addressing lipid levels such as LDL, triglycerides, and HDL cholesterol according to the 10-year calculated Framingham risk, and eating five servings of fruits and vegetables per day.8,9 and 10


Inpatient hyperglycemia.

Sometimes, when patients are acutely ill, they may develop what is called inpatient hyperglycemia. This can happen in patients who have latent diabetes, prediabetes, or are just at risk for diabetes development but are normally glucose-tolerant. It is unclear how frequently this leads to persistent diabetes after the hospitalization, but inpatient hyperglycemia is a bad prognostic sign that reflects decreased survival in the critical care units.11 It may be a harbinger of future diabetes if the patient survives. No systematic studies of long-term follow-up for patients with inpatient hyperglycemia have been done.


CLINICAL MANIFESTATIONS OF DIABETES MELLITUS

Clinical manifestations of diabetes mellitus could be acute (diabetic ketoacidosis or hyperosmolar hyperglycemic state) or chronic. The chronic complications manifest as microvascular (retinopathy, neuropathy, or nephropathy) or macrovascular (cerebrovascular disease, coronary artery disease, or peripheral vascular disease) disease. Other complications are susceptibility to infections and connective tissue disorders. Positive correlations were found between glycemic control (as measured by the A1C level) and prevalence and incidence of diabetic microvascular complications. Prospective randomized trials have shown that intensive control of blood glucose significantly reduces the risk of microvascular complications in both type 1 and type 2 diabetes. The effect of tight glucose control on macrovascular complications in the absence of intensified control of other macrovascular risk factors is presently controversial.12 It is known, however, that tight control of other CVD risk factors such as hypertension and elevated lipids does significantly reduce risk of fatal and nonfatal macrovascular events in both type 1 and type 2 diabetes patients. This reduction in risk was reported to be 20% to 50% with blood pressure control, 25% to 55% with lipid control, but only 10% to 20% with tight glucose control.12 A comprehensive approach including tight glucose control and control of other CVD risk factors was reported to lower both micro- and macrovascular complications by 35%.13 Unintended and adverse tight glucose control effects could be hypoglycemia, weight gain, and possible short-term worsening of proliferative retinopathy, especially and mostly when the patients require insulin, such as patients with type 1 or longstanding type 2 disease. Of particular concern is the effect of hypoglycemia on macrovascular event rates and outcomes.12








TABLE 32.3 Criteria for testing for diabetes in asymptomatic adult individuals

















1)

TESTING SHOULD BE CONSIDERED IN ALL ADULTS WHO ARE OVERWEIGHT (BMI ≥ 25 KG/M2)* AND HAVE ADDITIONAL RISK FACTORS:


  • Physical inactivity



  • First-degree relative with diabetes



  • Members of a high-risk race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander)



  • Women who delivered a baby weighing > 9 lb or were diagnosed with GDM



  • Hypertension (≥140/90 mmHg or on therapy for hypertension)



  • HDL cholesterol level <35 mg/dl (0.90 mmol/l) and/or a triglyceride level >250 mg/dl (2.82mmol/l)



  • Women with polycystic ovary syndrome (PCOS)



  • A1C ≥5.7%, IGT, or IFG on previous testing



  • Other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosis nigricans)



  • History of CVD


2)

IN THE ABSENCE OF THE ABOVE CRITERIA, TESTING FOR DIABETES SHOULD BEGIN AT AGE 45 YEARS


3)

IF RESULTS ARE NORMAL, TESTING SHOULD BE REPEATED AT LEAST AT 3-YEAR INTERVALS, WITH CONSIDERATION OF MORE FREQUENT TESTING DEPENDING ON INITIAL RESULTS AND RISK STATUS.


Adapted from American Diabetes Association: clinical practice recommendations. Diabetes Care. 2011;34(suppl 1). At-risk BMI may be lower in some ethnic groups










TABLE 32.4 Recommendations for Glycemic Control during Chronic Out-patient Management














































A1C

<7.0%*


Pre-prandial capillary plasma glucose

90-130 mg/dl


Peak postprandial capillary plasma glucose (Post-prandial glucose measurements should be made 1-2 h after the beginning of the meal)

180 mg/dl


Key concepts in setting glycemic goals are as follows:


•

A1C is the primary target for glycemic control


•

Goals should be individualized based on:



– duration of diabetes

– known cardiovascular disease or advanced micro-vascular complications

– age/life expectancy

– hypoglycemia unawareness

– co-morbid conditions

– individual patient considerations

• Certain populations (children, pregnant women, and elderly) require special considerations

• More or less stringent glycemic goals may be appropriate for individual patients

• Post-prandial glucose may be targeted if A1C goals are not met despite reaching pre-prandial goals


Adapted from American Diabetes Association: clinical practice recommendations. Diabetes Care. 2011;34(suppl 1).



Treating hyperglycemia to achieve target (outpatient management).

It is currently recommended to aim for tight glucose control as early as possible in the course of diabetes treatment (Table 32.4).1 The target level recommended by the American Diabetes Association (ADA) is A1C<7% or as close to normal as is safely possible to achieve.1 The A1C should be tested every 6 months if the value is at target or every 3 months when not at target or when treatment changes.

Levels of A1C together with the prevalence of hypoglycemia will dictate the management of glucose control. Correlation of A1C with average glucose level is seen in Table 32.5

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May 27, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Diabetes Mellitus in the Cardiac Care Unit

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