Blood Glucose

The fasting plasma glucose (FPG) level is assessed by a simple blood test after the person has not eaten for 8 hours. A normal FPG level is between 70 and 100 milligrams per deciliter (mg/dL).¹ A fasting glucose level between 100 and 125 mg/dL identifies a person who is prediabetic.¹ Even these individuals are at increased risk for complications of diabetes, such as coronary heart disease and stroke. A FPG level of 126 mg/dL (7 millimoles per liter [mmol/L]) or higher is diagnostic of diabetes (Table 32-1). In nonurgent settings, the test is repeated on another day to ensure that the result is accurate. After a meal, the concentration of glucose increases in the bloodstream. Recommended postprandial blood glucose levels should not exceed 180 mg/dL (10 mmol/L).¹

All critically ill patients must have their blood glucose levels monitored frequently while in the hospital. Clinical practice guidelines from the American Association of Clinical Endocrinologists (AACE) and the American Diabetes Association (ADA) recommend instituting insulin therapy when the blood glucose is greater than 180 mg/dL in critical illness.³ A target blood glucose range of 140 to 180 mg/dL is recommended.³

When a continuous insulin infusion is administered, point-of-care blood glucose testing is performed hourly or according to hospital protocol by the critical care nurse to achieve and maintain the blood glucose within the target range.³

Hypoglycemia is defined as a blood glucose level below 70 mg/dL (3.9 mmol/L).1,3 A complication of intensive glucose control is that hypoglycemic episodes may occur more frequently both in the hospital and with self-management of glucose levels in diabetes.³

Before discharge to home, patients with diabetes should be taught to monitor their blood glucose levels.⁴ Maintaining blood glucose within the normal range is associated with fewer long-term diabetes related complications.⁴ Laboratory blood tests and point-of-care or self-monitoring of blood glucose represent the standard of care for management of diabetes. Unfortunately, home monitoring of blood glucose is not the norm despite research evidence that maintaining blood glucose levels as close to normal as possible prolongs life and reduces complications.

Urine Glucose

Testing the urine for glucose is not recommended for patients with diabetes because too much variation exists in the threshold for glucose when diabetes-related kidney damage has occurred. Urine glucose measurements are affected by variation in fluid intake, reflect an average glucose level, not a specific point in time, and are altered by some medications. Urine glucose testing does not offer any help in the identification of hypoglycemia. For all of these reasons, urine glucose testing is never to be used.

Glycated Hemoglobin

Blood testing of glucose is useful for daily management of diabetes. However, a different blood test is used to achieve an objective measure of blood glucose over an extended period. The glycated hemoglobin test, also known as glycosylated hemoglobin (HbA_1C or A_1C) provides information about the average amount of glucose that has been present in the patient’s bloodstream over the previous 3 to 4 months. During the 120-day life span of red blood cells (RBCs; erythrocytes), the hemoglobin within each cell binds to the available blood glucose through a process known as glycosylation. Typically, 4% to 6% of hemoglobin contains the glucose group A_1C. A normal A_1C value is less than 5.4%, with an acceptable target level for diabetic patients below 6.5%.1,2,5 The A_1C value correlates with specific blood glucose levels as shown in Table 32-2.^1,2 The American Diabetes Association recommends use of the A_1C value both during initial assessment of diabetes mellitus, and for follow-up to monitor treatment effectiveness.¹

Blood Ketones

Ketone bodies are a byproduct of rapid fat breakdown. Ketone blood levels rise in acute illness, fasting, and with sustained elevation of blood glucose in type 1 diabetes in the absence of insulin. In diabetic ketoacidosis (DKA), fat breakdown (lipolysis) occurs so rapidly that fat metabolism is incomplete, and the ketone bodies (acetone, beta-hydroxybutyric acid, and acetoacetic acid) accumulate in the blood (ketonemia) and are excreted in the urine (ketonuria). It is recommended that all patients with diabetes perform self-test, or have their blood or urine tested, for the presence of ketones during any alteration in level of consciousness or acute illness with an elevated blood glucose.⁶ A blood test that measures beta-hydroxybutyrate, the primary metabolite of ketoacidosis, provides the most accurate measurement.^6,7 Self-test meters to measure blood ketones from a fingerstick are now available.⁶

Elevated levels of ketones (ketonemia) may be detected by a fruity, sweet-smelling odor on the exhaled breath. This distinctive breath odor derives from the elimination of acetone as part of the compensatory response to maintain a normal pH.

Urine Ketones

Ketones are eliminated in the urine, and urine may be tested for ketones. Ketonuria is retrospective and indicates that blood ketones were or are elevated.6,7 Ketonuria may also occur in fasting and starvation states.

Hydration Status

The nurse determines the effectiveness of ADH production by conducting a hydration assessment. A hydration assessment includes observations of skin integrity, skin turgor, and buccal membrane moisture. Moist, shiny buccal membranes indicate satisfactory fluid balance. Skin turgor that is resilient and returns to its original position in less than 3 seconds after being pinched or lifted indicates adequate skin elasticity. The skin over the forehead, clavicle, and sternum is the most reliable for testing tissue turgor because it is less affected by aging and more easily assessed for changes related to fluid balance. The skin in the groin and axilla is slightly moist to touch in a well-hydrated patient. In older patients, these typical assessment findings may be absent.

Other indicators that the patient’s hydration status is adequate for metabolic demands include a balanced intake and output and absence of thirst. Absence of thirst, however, is not a reliable indicator of dehydration in those with decreased thirst mechanisms such as the older or critically ill patients. Absence of abrupt changes in mental status may also indicate normal hydration. Other indicators of normal hydration include absence of edema, stable weight, and urine specific gravity that falls within the normal range (1.005 to 1.030).

Vital Signs

Changes in heart rate, blood pressure, and central venous pressure (when available) are useful to determine fluid volume status. Blood pressure and pulse are monitored frequently. Decreased blood pressure with increased pulse is characteristic of hypovolemia, whereas elevated blood pressure and a rapid, bounding pulse may indicate hypervolemia. Orthostatic hypotension, which occurs when intravascular fluid volume decreases, is identified by a drop in systolic blood pressure of 20 mm Hg or a drop in diastolic blood pressure of 10 mm Hg when the patient changes position from lying to standing.

Weight Changes and Intake and Output

Daily weight changes coincide with fluid retention and fluid loss. Sudden changes in weight can result from a change in fluid balance; 1 L of fluid lost or retained is equal to approximately 2.2 pounds (lb), or 1 kilogram (kg), of weight gained or lost. To use weight as a true determinant of the fluid balance, all extraneous variables are eliminated, and the same scale is used at the same time each day. Precise measurement and notation of intake and output are used as criteria for fluid replacement therapy.

Serum Antidiuretic Hormone

The normal serum ADH range is 1 to 5 picogram per milliliter (pg/mL). Prior to ADH measurement, all medications that may alter the release of ADH are withheld for a minimum of 8 hours. Common medications that affect ADH levels include morphine sulfate, lithium carbonate, chlorothiazide, carbamazepine, oxytocin, and selective serotonin reuptake inhibitors (SSRIs). Nicotine, alcohol, positive-pressure and negative-pressure ventilation, and emotional stress also influence ADH.

Serum ADH levels are then compared with the blood and urine osmolality to differentiate syndrome of inappropriate antidiuretic hormone (SIADH) from central diabetes insipidus (DI). Increased ADH levels in the bloodstream compared with a low serum osmolality and elevated urine osmolality confirms the diagnosis of SIADH. Reduced levels of serum ADH in a patient with high serum osmolality, hypernatremia, and reduced urine concentration signal central DI. Chapter 33 provides more information about SIADH and DI.

Serum and Urine Osmolality

Values for serum osmolality in the bloodstream range from 275 to 295 milliosmole per kilogram of water (mOsm/kg H₂O). Osmolality measurements determine the concentration of dissolved particles in a solution. In a healthy person, a change in the concentration of solutes triggers a chain of events to maintain adequate serum dilution. The most accurate measures of the body’s fluid balance are obtained when urine and blood samples are collected simultaneously.

Increased serum osmolality stimulates the release of ADH, which reduces the amount of water lost through the kidney. Body fluid is thus retained at the kidney tubules and collecting ducts to dilute the particle concentration in the bloodstream.

Decreased serum osmolality inhibits the release of ADH. The kidney tubules increase their permeability, and fluid is eliminated from the body in an attempt to regain normal concentration of particles in the bloodstream. Urine osmolality in the person with normal kidneys depends on fluid intake. With high fluid intake, particle dilution is low but will increase if fluids are restricted. The expected range for urine osmolality is, therefore, wide, ranging from 50 to 1400 mOsm/kg.