Chapter 46 – Management of Patients with Diabetes
-diabetes is a group of metabolic diseases characterized by hyperglycemia resulting from defects in
insulin secretion, insulin action, or both.
Epidemiology: ethnic and racial minority populations are disproportionately affected by diabetes.
Compared with Caucasians, African Americans, native Americans, and Hispanics are more likely to
develop diabetes and are at greater risk for many of the complications, and higher death rate. Diabetes is
the leading cause of nontraumatic amputations, and end stage kidney disease, 7th leading cause of death,
leading cause of blindness in adults 18-64
Classification: type 1 diabetes, type 2 diabetes, gestational diabetes, latent autoimmune diabetes of adults
(LADA). Except for type 1 diabetes, patients may move from different types of diabetes (from gestational
to type 2). Prediabetes is classified as impaired glucose tolerance (IGT) or impaired fasting glucose
(IFG) and refers to a condition in which blood glucose concentrations fall between normal levels and
those considered diabetic levels.
Risk factors for diabetes:
 over age 30 for type 2, under age 30 for type 1
 HDL lower than 35, triglyceride over 250
 History of gestational diabetes, delivery of baby over 9lbs
 Hypertension
 Family history of diabetes
 Obesity, BMI over 30
 Impaired fasting glucose, impaired glucose tolerance
 Race/ethnicity (black, Hispanic, native, Asian, pacific)
Pathophysiology: insulin is a hormone secreted by beta cells, which are one of four types of cells in the
islet of Langerhans in the pancreas. Insulin is an anabolic (storage hormone). When a person eats a meal,
insulin secretion increases and moves glucose from the blood into muscle, liver, and fat cells. Insulin has
the following actions: transports and metabolized glucose for energy, stimulates storage of glucose in the
liver and muscle(in the form of glycogen), signals liver to stop the release of glucose, enhances storage of
dietary fat in adipose tissue, accelerates transport of amino acids into cells, inhibits the breakdown of
stored glucose, protein and fat. During fasting, the pancreas continuously releases a small amount of
insulin (basal insulin) and glucagon when blood glucose levels decrease. Insulin and glucagon together
maintain a constant level of glucose in the bloodstream by stimulating the release of glucose from the
liver.
Type 1 diabetes: characterized by the destruction of pancreatic beta cells, combined genetic,
immunologic and possibly environmental factors are thought to contribute to beta cell destruction. People
do not inherit type 1, but rather have a genetic predisposition or tendency towards developing type 1.
There is evidence of autoimmune response in type 1 diabetes, where antibodies attack the normal cells of
the body, including beta cells in pancreas and endogenous insulin. Destruction of beta cells results in
decrease insulin production, increased glucose production by the liver and fasting hyperglycemia.
Glucose derived from food cannot be stored in the liver but instead remains in the bloodstream and
contributes to postprandial hyperglycemia. If the concentration of blood glucose exceeds the renal
threshold for glucose which is 180 to 200, the kidneys cannot reabsorb all of the filtered glucose:
glycosuria occurs (glucose in the urine). When excess glucose is excreted in the urine, it is accompanied
by excess loss of fluid and electrolytes (osmotic diuresis). Fat breakdown occurs, leading to increase in
ketones, a highly acidic substance formed when the liver breaks down fatty acids in the absence of
insulin. Diabetic ketoacidosis (DKA) a metabolic derangement that occurs most commonly in persons
with type 1, happens bc deficiency of insulin. Highly acidic ketones are formed, and metabolic acidosis
occurs. Three major metabolic derangements are: hyperglycemia, ketosis, and metabolic acidosis. DKA is
common preceded by a day or more of polyuria, polydipsia, nausea, vomiting and fatigue, can lead to
stupor and coma if not treated. The breath has a fruit odor due to presence of ketone acids.
Type 2 diabetes: occurs more commonly among people who are 30yrs + and obese, although now seen
in younger humans because of increasing rates of childhood obesity. Two main problems related to
insulin in type 2 diabetes are: insulin resistance and impaired insulin secretion. In type 2, intracellular
reactions to insulin are diminished, making insulin less effective at stimulating glucose uptake by the
tissues and at regulating glucose release by the liver. To overcome insulin resistance and prevent the
buildup of glucose in the blood, increased amounts of insulin must be secreted to maintain the glucose
level at the a normal level. If beta cells cannot keep up with the increased demand for insulin, glucose
levels rise and type 2 develops. Insulin resistance can lead to metabolic syndrome, which is a
constellation of symptoms including: hypertension, hypercholesterolemia, abdominal obesity. Despite
impaired insulin resistance, there is enough insulin to prevent the breakdown of fat and production of
ketones. DKA does not typically occur in type 2, uncontrolled type 2 can lead to hyperglycemic
hyperosmolar syndrome (HHS). Pancreas: impaired insulin secretion, GI absorption of glucose, Liver:
increase basal hepatic glucose production, Muscle: decreased insulin stimulated glucose uptake.
Type 2 is a slow progressive glucose intolerance, it can be undetected for years. Symptoms: fatigue,
irritability, polyuria, polydipsia, poor healing skin wounds, vaginal infections, or blurred vision.
Consequence of undetected type 2 is eye disease, peripheral neuropathy, peripheral vascular disease).
Gestational diabetes: any degree is glucose intolerance with its onset during pregnancy. Secretion of
placental hormones cause insulin resistance, usually in second or third trimester. Women who are obese
or have family history of diabetes are more likely to experience. Women’s glucose should be screened
throughout pregnancy. Initial management includes dietary modifications and blood glucose monitoring,
most women can control gestational diabetes with lifestyle modifications, some may need insulin. Target
levels during pregnancy are 140 to 180. After delivery, blood glucose results to normal, some may
develop type 2 later in life.
Latent Autoimmune Diabetes of Adults (LADA): subtype of diabetes in which the progression of
autoimmune beta cells destruction in the pancreas is slower than type 1 and type 2. Patients are at high
risk for becoming insulin dependent. Patients usually are less than 50yrs, BMI less than 25, history of
autoimmune disease, acute symptoms.
Prevention: type 2 can be prevented with lifestyle changes, weight reduction, increase exercise, type 2
can be prevented and delayed in persons who are high risk.
Clinical manifestations: dependent of the patients level of hyperglycemia. Classic clinical manifestations
include the three P’s: polyuria(increased urination), polydipsia(increased thirst, occurs as a result of the
excess loss of fluid associated with osmotic diuresis), polyphagia(increased appetite, results from
catabolic state induced by insulin deficiency and the breakdown of proteins and fats). Other symptoms
can include: fatigue, weakness, sudden vision changes, tingling or numbness in hands and feet, dry skin,
skin lesions and wounds that are slow to heal, recurrent infections. Onset of type 1 can be associated with
weight loss, nausea, vomiting, abdominal pain, if DKA has developed.
Criteria for diagnosis of diabetes:
 Symptoms of diabetes plus casual plasma glucose concentration equal to or greater than 200.
Casual is defined as any time of day without regard to time since last meal. The classic symptoms
of diabetes include the polyuria, polydipsia, unexplained weight loss.
 Fasting plasma glucose greater than or equal to 126. Fasting is defined as no caloric intake for at
least 8hrs.
 Two-hour post load glucose equal to or greater than 200 during an oral glucose tolerance test. The
test should use a glycose load containing the equivalent of 75g anhydrous glucose dissolved in
water.
 Hemoglobin A1C greater than or equal to 6.5%
Assessment and Diagnostic Findings: an abnormally high blood glucose level is the basic criteria for
diagnosing diabetes, plus others listed above.
Gerontologic Considerations: diabetes is particularly prevalent in older adults, type 2 diabetes is 7th
leading cause of death, effects 20% of older adults, high prevalence in African Americans, early detection
is important.
Medical Management: goal is diabetes treatment is to normalize insulin activity and blood glucose
levels to reduce the development of complications. Intensive glucose control dramatically reduces the
development and progression of complications such as retinopathy (damage to small blood vessels that
nourish the retina), nephropathy(damage to kidney cells), neuropathy(damage to nerve cells.) Intensive
treatment: 3-4 insulin injections per day, or an insulin pump plus frequent BG monitoring. Therapeutic
goal for diabetes is to achieve euglycemia (normal blood glucose) without hypoglycemia.
Diabetes management has five components:
Nutrition therapy: nutrition, meal planning, weight control and increased activity are the foundation of
diabetes management. Most important objective is to control total caloric intake to maintain reasonable
body weight, control of BG, and normal lipids and BP to prevent heart disease. Medical nutrition
therapy(MNT): usually given by a registered dietician, nutritional therapy prescribed for management of
diabetes. For patients who have diabetes and are obese, weight loss is the key to treatment. Meals should
not be skipped, pacing food intake throughout the day decreases demand on the pancreas. Meal plans
must consider the patients food preferences, lifestyle, usual eating times, and ethnic and cultural
background. Remaining consistent levels of carbohydrates and calories at each meal is important. Meal
plan for diabetes includes how many calories come from carbs, proteins, and fats. Recommendations:
50% to 60% carbs, 20% to 40% fat, 10% to 20% protein. Simple sugars, sweets, only 10% of diet because
high in fat and lack vitamins, minerals and fiber. Fats: reducing to 30% of total calories, 10% saturated
fat, cholesterol to 300mg/day. Protein: nonanimal is good, beans, whole grains, protein can be reduced in
those with early-stage kidney disease. Fiber: increase fiber improves blood glucose, decreases need for
insulin, lowers cholesterol and LDL. Two types of fiber: soluble and insoluble. Soluble: beans, oats,
fruits, lowers BG and lipids, slows stomach emptying. Insoluble fiber: whole grain bread, veggies,
increases satiety. Sudden increase in fiber, may require adjusting insulin or oral antidiabetics, can lead to
nausea, diarrhea, flatulence, and constipation if not enough fluid. to educate about diet principles and help
in meal planning, foods are organized in groups with common characteristics, like calories or effect on
blood glucose. Exchange lists: foods on one list may be interchanged with one another, allowing for
variety while maintaining as much consistency as possible in the nutrient content of foods. Nutrion labels
help with insulin planning, 1 unit of insulin for 15g of carbs. Counting carbs is useful for managing BG,
100% of carbs are converted to glucose, only 50% of protein are converted to glucose. Carb budget for
meals, not perfect but helps manage, some foods are digested differently. My plate is used only as a first
step educational tool for patients who are learning to control food portions and how to identify which
foods contain carbs, protein and fats. Glycemic index: used to describe how much a given food increases
the blood glucose level compared with an equivalent amount of glucose. Used to avoid sharp, rapid
increases in BG after eating. Combining starch with protein tends to slow absorption, eating raw foods
have lower GI than cooked or puree, whole fruit is better than juices due to fiber. Alcohol is absorbed
before other nutrients and does not require insulin for absorption, large amounts can be converted into fats
which increases risk for DKA. Patient with diabetes consumes alcohol on empty stomach can lead to
hypoglycemia, can also impair ability to notice signs and symptoms of hypoglycemia, combine food with
alcohol. One bev for women, 2 for men. Artificial sweeteners are okay, nutritive and nonnutritive.
Nutritive sweeteners have calories: fructose, sorbitol, xylitol, provide calories in amounts similar to table
sugar, cause less spike in blood sugar than sucrose. Cause less elevation in blood sugar. Nonnutritive
sweeteners have little to no calories, used in food products, minimal or no elevation in BG. Foods labeled
sugar free, may still have similar calories to products containing real sugar, still limit intake, must
carefully read labels of health foods closely.
Exercise: exercise is extremely important in diabetes management because of its effects on lowering
blood glucose and reducing cardiovascular risk factors. Exercise lowers blood glucose levels by
increasing the uptake of glucose by body muscles and by improving insulin utilization. Increase
circulation and muscle done. Strength training, weightlifting, can increase lean muscle mass, increasing
resting metabolic rate. Exercise also increases HDL and decreases triglyceride levels. A person with
diabetes should engage in regular exercise, exercises must be altered in those with complications such as
neuropathy, CVD. A slow gradual increase in the exercise period is encouraged, walking is great. Stress
test is recommended before starting exercise, risk factors are: hypertension, obesity, high cholesterol,
sedentary lifestyle, male, smoking, heart disease. Exercising with high blood sugar increases the secretion
of glucagon, even higher blood glucose. The physiologic decrease in circulating insulin that normally
occurs with exercise cannot occur in patients treated with insulin, they should eat a 15g carb snack before
exercising to prevent hypoglycemia. Patient should also eat post exercise. In type 2 patients who are
overweight or are obese, exercise in addition to dietary management improves blood glucose metabolism
and enhances loss of body fat. Physical fitness in the older adult population with diabetes may lead to
improved glycemic control, decreased risk for vascular disease, improved quality of life. Physical
therapists can do an eval on what is most appropriate for older adult.
Monitoring: blood glucose monitoring is a cornerstone of diabetes management, and self monitoring of
blood glucose (SMBG) levels have dramatically altered diabetes care. Allows for detection and
prevention of hypoglycemia and hyperglycemia and plays a crucial role in normalizing blood glucose
levels, which reduces risk of long term diabetic complications. Plasma glucose values are 10% to 15%
higher than whole blood glucose values, some strips provide whole blood or plasma results. Every 6 to 12
months should test blood glucose levels to compare with at home tests, have their testing methods
observed. For patients not taking insulin, SMBG is helpful for monitoring effectiveness of exercise, diet,
and oral antidiabetic agents. Should self monitor 2-4 times daily, before meals to determine dose, when
hypo or hyperglycemia is suspected, changes in medications, activity, diet, stress, illness. Patients should
keep a log of BG testing to detect patterns. Test at bedtime and at 3am too, patients are more likely to
discontinue SMBG if they are not instructed on how to use the results to alter the treatment regimen.
Continuous glucose monitoring (CGM) an advanced way that people with diabetes can monitor blood
glucose levels. A sensor attached to a transmitter is inserted subq in the abdomen or back of arm, sensors
are replaced every 7 to 14 days. Data is downloaded and analyzed, most useful for type 1. Glycated
hemoglobin: AIC, measure of glucose control for the past 3 months, when glucose levels are elevated,
glucose molecules attach to hemoglobin in red blood cells. The longer the amount of glucose in the blood
remains above normal, the more glucose binds to hemoglobin and higher A1C will be. Normal values are
from 4% to 6%, target range for diabetes is less than 7%. Ketones are by products of fat breakdown, and
they accumulate in the blood and urine. Ketones in the urine signal that there is a deficiency of insulin and
control of type 1 diabetes is deteriorating. When there is no insulin available, the body starts to
breakdown stored fat for energy. The patient may use a urine dipstick to detect ketonuria. Urine ketone
testing should be performed when blood sugar for type 1 is above 240 and during illness.
Pharmacologic therapy: insulin is secreted by the betal cells of the islets of Langerhans and lowers the
blood glucose level after meals by facilitating the uptake and utilization of glucose by muscle, fat and
liver cells. In the absence of adequate insulin, pharmacologic therapy is essential. In type 1 diabetes,
exogenous insulin must be given for life because the body loses the ability to produce insulin. In type 2
diabetes, insulin may be necessary on a long term basis to control glycose levels if meal planning and oral
agents are ineffective. Type 2 may require insulin temporarily during illness, infection, pregnancy,
surgery, or stressful event. There are numerous insulins available, vary according to time course of action,
species (source) and manufacturer.
Time course of action: insulin may be grouped in categories: onset, peak, and duration of action. Rapid
acting insulin produce a more rapid effect that is of shorter duration than regular insulin, eat no more than
5 to 15 mins after injection. Basal insulin is necessary to maintain blood glucose levels irrespective fo
meals. A constant level of insulin is necessary at all times. Intermediate acting insulins functions as basal
insulins but may have to be split into 2 injections to achieve 24 hour coverage. Short acting insulins are
called regular insulins, clear solution, given 15 mins before meal, alone or combination with long acting.
Can be administered IV. Intermediate acting insulins are called NPH insulin, are milky and cloudy,
doesn’t have to be taken before meal, but patient should eat around onset and peak. Peakless or basal
insulin, or long acting insulins are used as insulin that is absorbed ver slowly over 24 hours and can be
given once a day, cannot be mixed with other insulin. Once a day, at the same time each day, better to
take in the morning so they don’t forget before bed. Rapid and short acting insulins are expected to cover
the increase in glucose levels after meals, immediately after the injection, the intermediate-acting insulins
are expected to cover subsequent meals, and the long acting insulins provide a relatively constantly level
of insulin and act as a basal insulin.
Insulin regimens: there are two general approaches to insulin therapy: conventional and intensive,
patients can elarn to SMBG results and carb counting to vary insulin doses. Allows for flexibility in
timing and content of meals and exercise periods. Complex regiments require commitment, education,
and close follow up by health care team.
Conventional regimen: one approach is to simplify the insulin regimen as much as possible, aim to
avoid the acute complications of diabetes like hypoglycemia and symptomatic hyperglycemia. Simplified
regimen, one or more of short and intermediate acting insulin, patient should not vary meal patters and
activity levels. Would be appropriate for the elderly or who is unwilling to engage in a complex regimen.
Intensive regimen: a more complex regiment in order to achieve as much control over blood glucose
levels as is safe and practical. A more complex insulin regimen allows the patient more flexibility to
change insulin doses from day to day while their eating and activity patterns change, stress and illness.
The risk of severe hypoglycemia severely increases in those with an intensive treatment. The following
are not eligible for intensive: neuropathy, recurring hypoglycemia, blindness, CVD, ineffective selfcare
Complications of insulin therapy: local allergic reaction like redness, swelling, tenderness may appear
at injection site 1-2 hrs. after administering insulin, can resolve in a few hours or days if not insulin may
be changed. Systemic allergic reactions to insulin are rare, usually manifests as hives, treatment is
desensitization by giving small amounts of insulin every day. Insulin lipodystrophy refers to a localized
reaction occurring at injection site. Lipoatrophy is the loss of subcutaneous fat, appears as slight
dimpling or pitting. Lipohypertrophy: the development of fibrofatty masses at injection site, caused by
repeated use of area, rotation of sites is important. Patients can developed insulin resistance and may
require larger doses over time. Very few patients develop high levels of antibodies, and they usually have
interrupted insulin therapy for months, treatment is administering a more concentrated insulin.
Morning hyperglycemia is caused by an insufficient level of insulin.
 Dawn phenomenon: characterized by a relatively normal blood glucose level until
approximately 3am, when blood glucose levels begins to rise. The phenomenon is thought to
result from nocturnal surges in growth hormone secretion, which creates a greater need for insulin
in the early morning hours in patients with type 1 diabetes. Treated by changing time of injection
of evening intermediate acting insulin from dinnertime to bedtime.
 Insulin Waning: progressive rise in blood glucose from bedtime to morning. Treated by
increasing evening dose of intermediate or long acting insulin, or instituting a dose of insulin
before the evening meal if one is not already part of the treatment regimen
 Somogyi Effect: normal or elevated blood glucose at bedtime, early morning hypoglycemia, and
a subsequent increased blood glucose caused by the production of counter-regulatory hormones.
Treated by decreasing evening dose of intermediate acting insulin, or increasing bedtime snack.
Methods of Insulin delivery:
 Insulin pens: small 150 to 300 unit prefilled insulin cartridges that are loaded into a pen like
holder. A disposable needle is attached to the device for insulin injection, delivered by dialing in
a dose, insert the needle and inject insulin. Better than carrying insulin bottles and drawing it up.
 Jet injectors: deliver insulin through the skin under pressure in an extremely fine stream, more
expensive, peak and absorption rates may be different, absorbed faster, can cause bruising
 Insulin pumps: continuous subcutaneous insulin infusion involves the use of small, externally
worn devices called insulin pumps, mimics the functions of a healthy pancreas by providing
automated sstems that can adjust insulin delivery based on basal insulin every 5 minutes. Insulin
pumps contain a 3ml syiringe attached to a long 24-42 inch thin narrow lumen tube with a needle
attached at the end. Insert needle and secure with tape, changed every 3 days, pump worn on
clothes or in pocket. Risks include: occlusion of needle, insulin running out, battery depleted,
infection at needle site, pump is usually visible to others, must understand how to use the pump,
biggest risk is DKA is pump stops working unknowingly, should always have insulin on hand,
extra cost.
 Transplantation of pancreatic cells: transplantation of the whole pancreas or a segment of the
pancreas is being performed on a limited population, antirejection meds risk, implantation of
insulin produces islet cells too, only lasts 2 years, not widely available bc not enough organs.
Oral antidiabetic agents: may be effective for patients who have type 2 diabetes that cannot be
treated effectively with MNT and exercise alone. Oral antidiabetics include: sulfonylureas,
biguanides, alpha-glucosidase inhibitor, glitzamines, dpp4. Oral agents are prescribed as an addition
to other treatment modalities like MNT and exercise. Oral agents with insulin glargine at bedtime is
common in newly diagnosed with high blood glucose. Pramlintide is approved for both type 1 and
type 2, controls hyperglycemia and used with insulin, slows the rate at which food leaves the
stomach.
Managing glucose control in the hospital setting: hyperglycemia can prolong lengths of stay and
increase infection rates and mortality, occurs most often in patients with known diabetes.
 Blood glucose targets: 140 to 180
 Insulin (subcutaneous or IV) is preferred to oral antidiabetic agents to manage
hyperglycemia
 hospital insulin protocols, standardized hypoglycemic treatment, guidelines
 appropriate timing of blood glucose checks, meal consumption, and insulin dose are all
crucial for glucose control and to avoid hypoglycemia
Providing patient education: diabetes is a chronic illness that requires a lifetime of special self
management behaviors, multiple factors like MNT, physical activity, medication, physical and emotional
stress. Many health systems employ nurses and registered dieticians who specialize in diabetes education
and management. Information can be categorized into basic and then advanced complex. For type 2, must
teach meal planning, exercise, those taking medications need to know how to spot hypoglycemia, foot
care, eye care, more advanced teaching surrounding insulin pump, cgm, managing insulin doses
Assessing readiness to learn: when they are first diagnosed, they can be indenial, try to teach only what
is necessary, simple and direct info, take into consideration literacy level, financial resources and
healthcare, family support, daily schedule.
Storing insulin: when insulin is not in use, they should be refrigerated, temp extremes should be avoided,
should not be allowed to freeze or be kept in direct sunlight or hot car. Insulin vial in use should be kept
at room temp, have 1 month to use up. Cloudy insulin should be thoroughly mixed by gently inverting the
vial or rolling it between hands. Watch for expiration date, if insulin is frosted then it means its bound and
inactive and should not be used.
Selecting syringes: must be matched with the insulin concentration, three sized are available. Most
common in the US is 100 units per 1 ml.
 1ml syringe, 100 unit capacity
 0.5ml syringe, 50 unit capacity
 0.3ml syringe, 30 unit capacity
Mixing Insulins: when rapid or short acting are to be given simultaneously with longer acting insulin,
they can be mixed together in the same syringe. Longer acting needs to be mixed before drawing into
syringe. Regular insulin drawn up first, consistency in regimen is important to not make mistakes. Do
NOT inject cloudy into clear bc it will contaminate it. Premixed insulins are available in different ratios,
can pre draw syringes and keep in fridge for 3 weeks and then take out to get to room temp.
-Always push air into vial to make it easier to withdraw insulin.
Selecting and Rotating the Injection site: four main areas for injection are the abdomen, upper arms
(posterior surface), thighs (anterior surface) and hips. Speed of absorption is greatest in the abdomen and
decreases in other areas. Rotation of injection sites within an area is important to prevent damage to skin
and tissues. Do not inject insulin where you are going to work out because the drug will be absorbed
faster and cause hypoglycemia. Prepare the skin by cleaning with alcohol, let air dry. Insert the needle at
90 degrees for normal and overweight, might have to do 45 degrees for a very thin person. Place sharps in
a special box at home and then dispose of correctly, do not through in county trash.
Continuing and transitional care: to the degree to which patients interact with primary providers
depends on age, socioeconomic level, complications, type of diabetes, and comorbidities. Can participate
in support groups.
Acute complications of diabetes: three major acute complications of diabetes related to short-term
imbalances in blood glucose levels: hypoglycemia, DKA, and HHS.
Hypoglycemia: means low (hypo) sugar in the blood (glycemia) and occurs when blood glucose falls to
less than mg. It can occur when there is too much insulin or oral hypoglycemia agents, too little food, or
excessive physical activity. Can occur anytime during the day or night. Often occurs during meals, if
meals are delayed or snacks are omitted.
 Gerontologic considerations: in older patients’ hypoglycemia is a concern because older adult
frequently live alone and may not recognize symptoms, decreased kidney functions results in
longer period of time for oral hypoglycemics to be excreted, skipping meals may occur because
of decreased appetite or financial limitations, decreased visual acuity can lead to errors in insulin
administration
 Clinical Manifestations: can be grouped into two categories: adrenergic symptoms and central
nervous system symptoms.
In mild hypoglycemia, as blood sugar drops, the sympathetic nervous system is stimulated,
resulting in a surge of epi and norepi, cause symptoms such as sweating, tremor, tachycardia,
palpitation, nervousness and hunger.
In moderate hypoglycemia, the drop in blood glucose deprives the brain cells of needed fuel for
functioning. Signs of impaired function of the CNS include inability to concentrate, headache,
lightheadedness, confusion, memory lapses, numbness of the lips and tongue, slurred speech,
impaired coordination, emotional changes, irrational or combative behavior, double vision,
drowsiness.
In severe hypoglycemia, CNS function is so impaired that the patients’ needs the assistance of
another person for treatment of hypoglycemia. Symptoms include disoriented behavior, seizures,
difficulty arousing from sleep, or loss of consciousness.
 Assessment and Diagnostic Findings: symptoms of hypoglycemia may occur suddenly and vary
considerably from person to person. Decreased hormonal response to hypoglycemia may
contribute to lack of symptoms of hypoglycemia, occurs in patients who have had diabetes for
years. Can be related to autonomic neuropathy. As the blood glucose level falls, the normal surge
in adrenalin does not occur, and the usual adrenergic symptoms like sweating and shakiness don’t
occur. Hypoglycemia may not be detected until moderate or severe CNS impairment occurs.
Patients must perform SMBG on a frequent regular basis, esp before driving.
 Management: Immediate treatment must be given when hypoglycemia occurs, 15g-20g of a fast
acting concentrated source of carbs, fruit sugar juice, no need to add sugar. In adults whose
glucose level is less than 54 or who are unconscious and cannot swallow, an injection of glucagon
1mg can be given either subcutaneously or intramuscularly. Glucagon is a hormone produced by
the alpha cells of the pancreas that stimulates the liver to breakdown glycogen(stored glucose).
Injectable glucagon is packaged as a powder in a 1mg vial and must be mixed with a diluent
before injecting, can take up to 20 mins to regain consciousness. A carb snack should be given to
the patient once they awaken because glucagon onset is 8-10 mins and only lasts about 12-27
mins, replenish liver stores of glucose. Some patients experience nausea after glucagon, patient
should be turned to the side to prevent aspiration of vomit. Glucagon is sold prescription only and
should be part of the emergency supplies available to patients with diabetes who require insulin.
In hospitals, patients who cannot swallow or are unconscious, 25mL to 50mL of dextrose 50% in
water (D50W) is given IV. Effect is seen within minutes, can experience headache, pain at
injection site, ensure patency of IV bc 50% dextrose is irritation to veins.
 Patient Education: hypoglycemia is prevented by a consistent pattern of eating, administering
insulin, and exercising. Between meal and bedtime snacks may be needed to counteract the
maximum insulin effect. Patients should cover the time of peak activity of insulin by eating a
snack and by carrying snacks with them when they are being more active than usual. Patients
should wear tag that says they are diabetic. Teach family and friends how to identify signs and
symptoms of hypoglycemia. Patients should report severe hypoglycemic episodes in addition to
any increase in incidence, frequency, and severity to the primary provider.
Diabetic Ketoacidosis: caused by an absence or inadequate amount of insulin. This deficit in
available insulin results in disorders in the metabolism of carbohydrate, protein, and fat. Three main
clinical features of DKA are hyperglycemia, dehydration and electrolyte loss, acidosis.
 Pathophysiology: If the body does not have any insulin, the amount of glucose entering the
cell is reduced, and gluconeogenesis (the production and release of glucose by the liver) is
increased, which leads to hyperglycemia. In an attempt to rid the body of the excess glucose,
the kidneys excrete the glucose along with water and electrolytes (sodium, potassium). This
osmotic diuresis, which is characterized by polyuria, leads to dehydration and electrolyte loss.
Patients with severe DKA can lose up to 6.5L of water and up to 400-500mEq of sodium,
potassium and chloride in 24 hrs. Another effect of insulin deficiency is lipolysis which is the
breakdown of fat into free fatty acids and glycerol. The free fatty acids are converted into
ketone bodies by the liver. Ketone bodies are acids, their accumulation in the circulation due
to lack insulin leads to metabolic acidosis.
Three main causes of DKA are decreased or missed dose of insulin, illness or infection, and
undiagnosed and untreated diabetes (DKA might be the initial manifestation of type 1 in an
undiagnosed individual). Insulin deficiency can result from an insufficient dosage of insulin
that is prescribed, or the patient simply not injecting enough. When patients are sick, they eat
less and might assume that they need to take less insulin which can lead to DKA, in reality
they need the same amount if not more insulin while ill.
Lack of insulin leads to decreased utilization of glucose by the muscle, fat, and liver in
response the liver increases production of glucose (gluconeogenesis) which leads to
hyperglycemia, manifests as blurred vision and polyuria (an attempt by the kidneys to rid
itself of excess glucose, also excretes electrolytes and water), leads to dehydration which
ultimately leads to weakness, headache, and polydipsia (increased thirst).
Lack of insulin leads to the breakdown of fat for fuel, increases free fatty acids in the blood
which is converted into ketones, ketones manifest as acetone breath, poor appetite, and
nausea. Increased ketone bodies lead to acidosis which manifests as nausea, vomiting,
abdominal pain, and increased rapid respirations (Kussmaul breathing).
 Prevention: Preventing DKA that occurs due to illness, there should be ‘sick day rules’ that
include: never eliminate insulin doses when sick, attempt to consume small frequent meals of
simple sugars, drink enough fluids to prevent dehydration, blood glucose and urine ketones
must be assessed every 3-4 hours. If the patient cannot drink fluids without vomiting,
elevated blood glucose, or ketone levels, contact provider. Patients should have urine test
strips available, create a sick day kit.
 Clinical Manifestations: The hyperglycemia of DKA leads to polyuria, polydipsia, and
marked fatigue. The patient can also experience blurred vision, weakness, and headache, may
have orthostatic hypotension, weak pulse (if low fluid volume). The ketosis and acidosis of
DKA lead to GI symptoms: anorexia, nausea, vomiting, abdominal pain. Patient may have
acetone (fruity) breath, hyperventilation (kussmaul respirations) is the body’s attempt to
decreased the acidosis. Mental status can vary widely, patient can be alert, lethargic or
comatose.
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Assessment and Diagnostic Findings: Blood glucose levels may vary between 250-800, can
be higer, depends on degree of dehydration. The severity of DKA is not related to blood
glucose levels. Evidence of ketoacidosis is reflected in low serum bicarbonate (0 to 15) and
low PH (6.8 to 7.3). A low partial pressure of carbon dioxide (PaO2 10 to 30) reflects
respiratory compensation due to metabolic acidosis. Accumulation of ketone bodies is
reflected in blood and urine ketone measurements.
Sodium and potassium concentrations may be low, normal, or high depending on the amount
of dehydration. Increased levels of creatinine, blood urea nitrogen(BUN), and hematocrit may
be seen with dehydration.
Management: Management of DKA is aimed at correcting dehydration, electrolyte loss, and
acidosis before correcting the hyperglycemia with insulin.
Rehydration: in dehydrated patients, rehydration is important for maintaining tissue
perfusion. Fluid replacement increases the excretion of excess glucose by the kidneys. The
patient may need as much as 6 to 10 L of IV fluid to replace fluid losses caused by polyuria,
hyperventilation, diarrhea, and vomiting. Initially, 0.9% sodium chloride (normal saline) is
given at a rapid rate, 0.5 to 1L per hour for the first 2-4 hours. Half strength NS (.45%) is
hypotonic, and may be given to patients with hypertension or hypernatremia. After the first
few hours, half normal saline is the fluid of choice for continued rehydration, provided the
blood pressure is stable and the sodium level is not low. When blood glucose level reaches
300mg or less, the IV solution can be changed to dextrose 5% in water to prevent a decline in
blood glucose levels. Monitoring of fluid volume status involves checking vital signs, lung
assessment, I&Os. Monitor for signs of fluid overload in patients who are older, renal
impairment, or HF.
Restoring Electrolytes: the major electrolyte of concern during treatment of DKA is
potassium. The initial plasma concentration may be low, normal or high but it usually tends
to be high (hyperkalemia) from disruption of the cellular sodium potassium pump (due to
acidosis). Rehydration can affect potassium levels by lowering them, due to increase fluid
volume and urinary excretion of potassium. Insulin administration enhances the movement of
potassium from the extracellular fluid into the cells. Cautious but timely potassium
replacement is vital to avoid arrhythmias that may occur with hypokalemia. Extracellular
potassium levels decreased during DKA treatment, potassium must be infused even if the
plasma levels are normal. Check potassium ad ECGs every 2 hours during beginning of
treatment, potassium treatment is only withheld if patient has hyperkalemia is present or is
patient is not urinating.
Because a patients serum potassium level may drop quickly as a result of rehydration
and insulin treatment, potassium replacement must begin once potassium levels drop to
normal in the patient with DKA.
Reversing Acidosis: Ketone bodies (acids) accumulate as a result of fat breakdown, the
acidosis that occurs in DKA is reversed with insulin, which inhibits fat breakdown, ends
ketone production and acid buildup. Insulin is usually infused IV at a slow, continuous rate, 5
units per hour. Must measure hourly blood glucose. IV fluid with dextrose are given once
blood sugar levels reach 300 to prevent hypoglycemia during treatment. Regular insulin (only
type approved for IV) is usually infused separate from the rehydration solutions to allow
frequent changes in the rate. Insulin must be infused continuously until subq insulin can
resume, any interruption in insulin may result in ketones and worsening acidosis. Insulin drop
must not be stopped until subq therapy of insulin can be restarted! The rate or concentration
of dextrose can be increased to prevent hypoglycemia. Blood glucose levels are usually
corrected before the acidosis is corrected, so IV insulin may be continued for 12 to 24 hours
until bicarb level increased to atleast 15 to 18 mEq. Bicarbonate infusion is avoided to correct
acidosis because it can cause sudden and fatal drop in potassium levels. Continous insulin
infusion is usually sufficient for reversal of DKA.
When hanging the insulin drip, the nurse must flush the insulin solution through the
entire IV infusion set and discard the first 50mL of fluid. Insulin molecules adhere to
the inner surface of plastic IV infusion sets; therefore, the initial fluid may contain a
decreased concentration of insulin.
Hyperglycemic Hyperosmolar Syndrome: HHS is a metabolic disorder most often of type 2 diabetes
resulting from a relative insulin deficiency initiated by an illness that raises the demand for insulin. This is
a serious condition, hyperosmolality and hyperglycemia, with alterations of the sensorium (sense of
awareness). Ketosis is usually minimal or absent. The basic biochemical defect is the lack of effective
insulin (insulin resistance.) Persistent hyperglycemia causes osmotic diuresis, which results in losses of
water and electrolytes. To maintain osmotic equilibrium, water shifts from the intracellular fluid space to
extracellular fluid space. With glycosuria and dehydration, hypernatremia and increased osmolarity occur.
HHS occurs most often in older adults (50-70yrs) who have no history of diabetes or have type 2. HHS
can be traced to an infection, or an acute illness (stroke), medications that make hyperglycemia worse
(thiazides), or dialysis. What distinguishes HHS from DKA is that ketosis and acidosis generally do not
occur in HHS, because of the differences in insulin levels. In DKA, there is no insulin present and this
promotes breakdown of stored glucose, protein and fat, which leads to ketone bodies and ketoacidosis. In
HHS, the insulin level is too low to prevent hyperglycemia but it is high enough to prevent fat
breakdown. Patients with HHS do not have the ketosis-related GI symptoms. They may tolerate polyuria
and polydipsia until neurological changes prompt them to seek help.
 Clinical manifestations: the clinical picture of HHS is one of hypotension, profound
dehydration (dry mucous membranes, poor skin turgor), tachycardia, and variable neurologic
signs (alterations of consciousness, seizures, hemiparesis).
 Assessment and Diagnostic Findings: Diagnostic assessment includes a range of lab tests,
including blood glucose, electrolytes, BUN, CBC, serum osmolality, and arterial blood gas
analysis. Blood glucose is greater than 600, the osmolality exceeds 320, and ketoacidosis is
absent. Electrolyte and BUN levels should be consistent with the clinical picture of severe
dehydration. Mental status changes, focal neurologic deficits, and hallucinations are common.
Orthostatic hypotension + dehydration.
 Management: the overall approach to treatment of HHS is similar to that of DKA: fluid
replacement, correction of electrolyte imbalances, and insulin administration. Because
patients is HHS are typically older, monitor volume and electrolyte status to prevent fluid
overload, HF, cardiac dysrhythmias. Fluid treatment is started with NS or 1/2NS, depending
on the patients sodium level. Potassium is added to IV fluids when urinary output is okay,
continuous ECG monitor and lab potassium. Extremely high blood glucose lowers as the
patient is rehydrated, insulin is not as important as it in treatment of HHS because its not
needed to reverse acidosis in DKA. Insulin is still given to treat hyperglycemia, and it
switched over to dextrose once BG is 250-300. It may take 3-5 days for neurologic symptoms
to clear, insulin may not be needed once acute hyperglycemia is resolved, patients will be on
oral antidiabetics or MNT. Frequent SBGM is important to prevent HHS.
Long-term complications of diabetes: Increased level of blood glucose plays a role in neuropathic
disease, microvascular complications, and risk factors contributing to macrovascular complications. Long
term complications are seen in both type 1 and type 2 but usually don’t occur within the first 5-10yrs of
diagnosis. Kidney(microvascular) disease is more prevalent in patients with type 1, and
cardiovascular(macrovascular are more prevalent in those older patients with type 2.
Macrovascular complications: Result from changes in the medium to large blood vessels. Blodo vessel
walls thicken, scleroses, and become occluded by plaque that adheres to the vessel walls. Eventually,
blood flow is blocked. They tend to occur in early age in patients with diabetes. Examples: coronary
artery disease, cerebrovascular disease, and peripheral vascular disease are most common. MI is twice as
common in men with diabetes and three times as common in women with diabetes. Increased risk of
stroke, cerebral blood vessels are affected too. Atherosclerotic changes in the large blood vessels of the
lower extremities are responsible for peripheral artery disease. Increased incidence of gangrene and
amputation of diabetics, neuropathy and impairments in wound healing also play a role. MNT and
exercise is important to mitigate risk, managing obesity, hyperlipidemia, hypertension, smoking
cessation.
Microvascular complications: diabetic microvascular disease is characterized by capillary basement
membrane thickening. The basement membrane surrounds the endothelial cells of the capillary. Increased
blood glucose levels react to thicken the basement membrane, kidneys and retina are affected.
 Diabetic retinopathy: the leading cause of blindness among people between 20 and 74yrs of age,
occurs in type 1 and type 2. People with diabetes are subject to many visual complications,
caused by changes in the small blood vessels in the retina, which is the area of the eye that
receives images and sends information about the images to the brain. The retina is richly supplied
with blood vessels of all kinds: small arteries and veins, arterioles, venules and capillaries.
Almost all patients with type 1 and type 2 have some degree of retinopathy after 20 years.
Preproliferative, a precursor, vascular changes and loss of nerve fibers. Proliferative retinopathy
prevents the greatest threat to vision and is characterized by new blood vessels growing that are
prone to bleeding, retinal detachment or bleeding causes vision loss. Clinical manifestations:
blurry vision, floaters, cobwebs, spotty or hazy vision, or complete loss of vision. Assessment and
diagnostic findings: visualization of the eye through dilated pupils. Medical management:
preventing is the cure, maintaining stable blood glucose is very important, controlling
hypertension, cessation of smoking, laser treatment. Nursing management: providing education,
eye exams, eye care regimens, blood glucose control, education! Once eye starts to deteriorate,
blindness is almost inevitable, but we can help patients cope and learn braille.
 Nephropathy: kidney disease, can lead to ESKD. If blood glucose levels are consistently high for
a long period of time, kidneys filtration mechanism is stressed. Clinical manifestations:
breakdown of insulin, frequent hypoglycemic episodes, changes in diet. If kidneys are starting to
fail, they break down insulin so the diabetic will need more of it. Assessment: albumin is the most
important blood protein that leaks into the urine when kidney function is diminishing. Urine
should be checked annually. Management: maintaining normal blood glucose levels, control
hypertension, prevent UTIs, low sodium diet, low protein diet. For chronic ESKD, dialysis or
transplant are the only options.
Diabetic Neuropathies: refers to group of diseases that affect all types of nerves, including peripheral,
autonomic and spinal nerves. Prevalence increases with age of patient and duration of the disease.
 Peripheral neuropathy most commonly affects the distal portions of the nerves, lower extremities,
both sides of the body symmetrically and may spread. Capillary basement thickening,
demyelination of the nerves which is related to hyperglycemia. Clinical manifestations: about half
patients do not have symptoms, initial symptoms may include tingling, burning sensation, feet
can become numb, decrease in proprioception, pain and temp, can lead to falls and foot
infections, joints can also become deformed from abnormal weight distribution. Decrease in
tendon reflexes and sensations. Management: intensive insulin therapy and control of blood
glucose levels delays the development of neuropathy. Pain can persists for years, meds are given.
 Autonomic Neuropathies: three manifestations are related to the cardiac, GI, and renal. Cardio
symptoms: tachy HR, orthostatic hypotension, painless MI, cardio health worsens with diabetes.
GI: delayed gastric emptying, bloating, nausea, vomiting, constipation, diarrhea. Renal: urinary
retention, bladder fullness sensation, can get UTIs.
 Other issues: hypoglycemic unawareness, sudomotor neuropathy (decrease in sweating in lower
extremities, so super sweaty at upper extremities). Sexual dysfunction, erectile, reduced vaginal
lubrication, UTIs. Management: alleviating symptoms and management of risk factors. Lower
body elastic garments to help blood flow, low fat diet can help delayed gastric emptying.
Foot and Leg Problems: Amputations are preventable is patients are taught appropriate foot care.
Complications of diabetes that contribute to the increased risk of foot problems and infections include:
neuropathy (loss of pain and pressure sensation), peripheral vascular disease (poor circulation in lower
extremities), immunocompromise (hyperglycemia impairs the ability of leukocytes to destroy bacteria).
Must inspect feet daily, there may be a lot that the patient might not feel or be aware of and it can
progress rapidly. Amputation may be needed to prevent the spread of infection. Medical management:
feet of a patient should be examined during every health visit, look for pressure areas, calluses, thick
toenails, see a podiatrist. Nursing management: educating patients about proper foot care can preven
severe complications.
Special Issues in Diabetes Care:
 Patients w/ Diabetes who are undergoing surgery: during long periods of stress, blood glucose
levels tend to increase because release of stress hormones, might need more insulin.
Hypoglycemia is also a risk if patient received morning insulin and is NPO for too long before
surgery. Frequent blood glucose monitoring is key, use if IV insulin and dextrose is common.
 Patients w/ Diabetes who are hospitalized: a lot of patients who are hospitalized have diabetes,
it’s a good importunity to provide extra teaching. Can be an opportunity to evaluate patients self
care skills and reinforce any teaching they may need. Causes of hyperglycemia: changes in usual
routine, medications, IV dex, inappropriate sliding scale, mismatched timing of insulin + meals.
Hypoglycemia: overuse of insulin, lack of change in insulin when npo is established, delayed
mail after insulin.
Common alterations in diet:
 Nothing by mouth: NPO, may need to eliminate rapid acting insulin and give less of intermediate
acting insulin, glucose testing is vital.
 Clear liquid diet: patients will receive more simple sugars as a result, watch insulin peak times
 Enteral tube feedings: contain more simple and less protein and fat, increased glucose levels,
watch for insulin, NPH every 12hrs and regular every 4-6hrs). Monitor BG frequently.
 Parenteral nutrition: can receive IV insulin or subq, monitor and give at regular intervals
Hygiene: oral hygiene and skin care, increase risk for periodontal disease, keep skin dry, turn patients,
check tingling and numbness of feet, deep tendon reflexes, skin breakdown, pressure points,
Stress: surgery, infections can lead to hyperglycemia which leads to DKA and HHS. Emotional stress can
also have negative impact on diabetic control. Might need more insulin.
Older adults: Careful monitoring for complications of diabetes in older adults is vital. Hypoglycemia is
especially dangerous because it may go undetected and result in falls. Dehydration is a concern in patients
who have chronically elevated blood glucose levels. Assessment for long-term complications, especially
eye and foot problems, is important. Avoiding blindness and amputation through early detection and
treatment of retinopathy and foot ulcerations may mean the difference between placement in a long-term
care facility and continued independent living for the older adult with diabetes.
Nursing management: frequently check BG, double check insulin orders, make sure its modified as
needed, order labs, check labs, watch closely! Always assess adherence of diabetic plan and treatment and
educate patient as needed.