TYPE 1 DIABETES MELLITUS
Type 1 diabetes is typically triggered by an autoimmune process in which the insulin-producing beta
cells of the pancreas are destroyed, resulting in an absolute lack of insulin. In children and young adults,
this process is usually rapid, with total insulin deficiency occurring within 1 year, after which lifelong
insulin therapy required. If the disease begins in adulthood, the autoimmune destruction of beta cells
has a more variable but generally slower time frame.
Adult patients with new autoimmune type 1 diabetes may retain some insulin-secreting ability for
years. Eventually, however, they develop total insulin deficiency. Once beta-cell destruction has
progressed to the point of total insulin deficiency, patients with type 1 diabetes require externally
delivered insulin (provided via a pump or injection) for the remainder of their lives.
Patients undergoing pancreatic resection as a result of cancer or other diseases of the pancreas may
also present with type 1 diabetes because of a lack of insulin after the surgical procedure. Like patients
diagnosed with type 1 diabetes caused by the autoimmune process, these patients will also require
lifelong insulin therapy.
There are both genetic and environmental factors involved in the development of type 1 diabetes. The
risk of developing type 1 diabetes increases if family members have type 1 diabetes or other associated
autoimmune disorders such as autoimmune thyroid disease, celiac disease, or Addison’s disease.
Environmental triggers also play a part in genetically sensitive individuals. Although the specific triggers
are not yet fully understood, they are thought to include viruses such as mumps, rubella, and Coxsackie
B4; toxic chemicals; and cytotoxins (substances that are toxic to and kill living cells).
Clinical Manifestations
Clinical manifestations caused by the hyperglycemia of type I diabetes are evident in many body
systems. Predominant features include polyuria, polydipsia, polyphagia, fatigue, and weight loss.
Polyuria, increased volumes of urine, is due to increased concentration of glucose in the urine,
or glucosuria.
Glucose is typically totally reabsorbed in the renal tubules. Hyperglycemia results in glucose excretion in
the urine, which creates an osmotic effect that effectively reduces water reabsorption into the renal
tubules, leading to excessive volume loss through the kidneys. Hyperglycemia also causes
hyperosmolality in the blood, which causes a shift of fluid from the intracellular space to the vascular
space. The loss of intracellular water combined with the volume loss through the kidneys creates
excessive thirst in the patient, or polydipsia.
The lack of insulin necessary to move glucose into the cells leads to the breakdown of proteins and fat
as a source of energy. This starvation of the cells leads to polyphagia, increased appetite. Despite an
increased appetite leading to consumption of large amounts of food, the continual breakdown of fats
and proteins leads to weight loss and fatigue.
Medical Management
Diagnosis
Type 1 DM in the nonpregnant adult is diagnosed by various methods:
• Hemoglobin A1c (glycosylated hemoglobin) value. The HgbA1c test measures the average blood
glucose concentration over time by measuring the amount of glucose that binds to red blood cells.
Reflecting the average life span of a red blood cell, the test gives an accurate indication of long-term,
time-averaged glucose levels over the 6 to 8 weeks prior to the HgbA1c blood draw. When blood
glucose concentrations are high, more hemoglobin is affected. On the day the HgbA1c is drawn, eating,
physical activity, or acute stresses do not affect the result, and the test can be done at any time of day
and does not require fasting. Because of these characteristics, it is a good tool to monitor the
effectiveness of insulin therapy as well as the patient’s compliance with diabetes management plan.
The HgbA1c levels do not show fluctuations, and swings between hypoglycemia and hyperglycemia
can be masked in the “average.” Measurement depends on the red cell survival and the composition of
red cell hemoglobin, so HgbA1c results are inaccurate in several clinical situations such as recent blood
loss or transfusions. In addition, it is not accurate in the setting of anemia and treatment with
erythropoietin, both of which are common in patients with diabetic renal disease.
• Fasting blood glucose. Fasting is defined as no caloric intake for at least 8 hours. Without adequate
oral intake, glucagon is released from the pancreas, facilitating the release of glycogen stores from the
liver and increasing circulating blood glucose levels. Normally, insulin is released, moving that glucose
into the cells, preventing hyperglycemia. Without adequate insulin, hyperglycemia results.
• 2-hr postprandial (after meals) or the oral glucose tolerance test (OGTT). This test is performed by
asking the patient to consume a beverage containing a glucose load, the equivalent of 75 g of
carbohydrate, after fasting for 8 to 12 hours. Blood samples are taken prior to consuming the drink to
get a fasting level, then again at 1 hour and 2 hours after consumption. The diagnostic value is based on
the blood glucose level 2 hours after consumption.
• Random blood glucose. A random blood glucose level of greater than or equal to 200 mg/dL in a
patient with classic symptoms of hyperglycemia or hyperglycemic crisis may be indicative of diabetes
mellitus.
Treatment
Successful treatment of type 1 DM involves several different strategies, including pharmacological
interventions, nutrition management, patient education and self-management, and detection and
prevention of complications. Nutrition, patient education and self-management, and detection and
prevention of complications are similar for both type 1 and type 2 DM, and are discussed under
management of type 2 DM later in this chapter. The focus here is on the pharmacological interventions
for type 1 DM.
Pharmacological Interventions
The primary pharmacological intervention used in the treatment of type 1 DM is insulin administered
subcutaneously. Oral administration of insulin is not effective because it is broken down and rendered
ineffective during the digestive process. The goal of treatment is to maximize glycemic control, the
maintenance of blood glucose levels within normal ranges in an effort to prevent the complications of
hyperglycemia. In setting glycemic goals, it is important to consider that the closer the goals are to
normal ranges, the lesser the risk of complications from diabetes.
The recommended guidelines for setting individualized targets focus on weighing the potential risks of
hypoglycemia with the benefits of tight glycemic control. Treatment goals should be determined and
reassessed periodically on the basis of patient-specific factors such as health status, adverse drug
reactions, adherence to treatment, and patient preferences. If glycemic goals are not met, the patient
should be assessed for knowledge, performance skills, as well as psychosocial, personal, or financial
barriers
Safety Alert
Insulin is a high-risk medication with a narrow therapeutic margin. Tight glycemic control increases the
risk of hypoglycemia in patients who rely on insulin and oral agents that stimulate the release of insulin
to manage their diabetes. The benefits of tighter glucose control may not outweigh the risks for some
patients. This includes patients with a limited life expectancy, those with comorbidities where a
hypoglycemic event will have more serious consequences, or those unwilling or unable to do the
monitoring necessary to prevent hypoglycemia. This risk is especially pronounced in patients with a
tendency toward hypoglycemia, such as the elderly, the malnourished, or those with renal or liver
disease.
An approach using a combination of long- or intermediate-acting insulin once or twice a day to
provide basal insulin is most effective in maintaining tight glycemic control. These approaches include
rapid- or short-acting insulin taken at mealtimes to cover the incoming carbohydrates, prandial
insulin or nutritional insulin and a “sliding scale” of additional supplemental or correctional insulin to
compensate for blood glucose elevations. The need for correctional insulin is determined by a random
blood glucose level done via finger stick immediately prior to eating. The prandial and correctional
insulins are then administered at the same time prior to eating. In hospitalized patients with
questionable or minimal oral intake, prandial and correctional insulins can be given immediately after
the meal to confirm adequate carbohydrate intake. This approach best mimics the way the healthy
pancreas releases insulin, but it does require multiple blood glucose evaluations (figure sticks) and
injections daily.
Subcutaneous insulin can be drawn up and administered via needle and insulin syringe, or it can be
administered through an insulin pen. If insulin syringes are used, it is important to match the syringe size
to the insulin concentration. The most typical insulin concentration is U-100, which means 100 units of
insulin per milliliter. U-100 insulin syringes come in several sizes: 1 mL that holds 100 units, 0.5 mL that
holds 50 units, and 0.3 that holds 30 units. The patient should choose the insulin syringe size according
to his or her insulin dosage. For example, using the small 0.3-mL syringe allows patients that are
prescribed very small doses to more accurately draw up their insulin. If insulin requirements are massive
because of extreme insulin resistance, a U-500 (500 units per milliliter) insulin concentration is available
by special order. In contrast to the insulin syringe and needle, the insulin pen allows the patient to dial in
the exact dosage, avoiding the potential errors inherent in measuring and drawing up insulin in the
traditional way.
An alternative approach to the administration of insulin is the use of continuous subcutaneous insulin
pumps. Insulin pumps provide the same delivery of basal and bolus insulin as the multiple injection
technique, but it is provided by a computer-driven device that delivers insulin according to instructions
programmed by the patient). The use of the subcutaneous insulin pump has been found to provide
better glycemic control, especially in patients with higher hemoglobin A1c levels indicating poor
glycemic control with traditional methods. Advantages of the pump include convenience and the ability
to deliver more precise dosages. Patients state that it allows better quality of life and more freedom
from the strict restrictions inherent in the traditional insulin administration methods. Disadvantages are
the expense, the need to “wear” the pump continuously, skin issues around the needle insertion site,
and potential complications if the pump malfunctions.
Some patients are unable or unwilling to manage the multiple daily blood glucose evaluations and
injections or the insulin pump. An alternative treatment plan is twice-daily finger sticks with twice-daily
insulin injections. This does not offer the same possibility of tight glycemic control as the other methods,
but it is less complicated and easier to manage. The insulin used is typically a mixture of rapid- and longacting insulin. This insulin can be administered via needle and syringe, or it is also available in an insulin
pen.
Methods for Assessing Glycemic Control
There are three methods of assessing glycemic control. Each method has advantages and drawbacks and
should not be used in isolation. The methods are:
• Self–monitoring of blood glucose
• Continuous blood glucose monitoring
• Monitoring of HgbA1c
Self–Blood Glucose Monitoring
Self–monitoring of blood glucose via finger stick provides a snapshot of blood glucose at a specific
instant in time. It can therefore provide timely feedback to the patient about the effect of his or her
behavior, health, and eating habits on the blood glucose level. In order for this method to be effective,
patients must receive instructions on the accurate testing procedure. The most common patient-related
error is inadequate blood sample size. The patient’s technique should be observed by a trained observer
on initiation of the plan of care and also should be reviewed annually or as indicated. Patients should be
taught the importance of documenting results. With a record of blood glucose levels, food intake, and
medication dosage, a diabetes educator can assist the patient in recognizing and interpreting blood
glucose patterns. With this information, the patient can learn to adjust insulin dosing, food intake, or
exercise and maximize glycemic control. As patients discover what works and what doesn’t, they can
gain an important sense of control over their blood glucose levels.
The frequency of self-monitoring of blood glucose in patients using insulin should be individualized on
the basis of frequency of insulin injections, hypoglycemic reactions, level of glycemic control, and
patient/provider use of the data to adjust therapy. Generally, patients with type 1 DM are advised to
check their blood glucose a minimum of before meals and at bedtime. Patients on insulin pumps often
check more frequently, especially during periods of medication adjustment.
Increased frequency of self-monitoring of blood glucose levels is recommended when:
• Therapy is being initiated or actively adjusted
• There is acute or ongoing illness
• There is hypoglycemia unawareness or an increase in hypoglycemia events
• Fasting and/or postprandial blood glucose levels are not consistent with HgbA1c
Continuous Glucose Monitoring
Continuous blood glucose monitoring systems use a tiny sensor inserted under the skin to check
glucose levels in interstitial fluid. The sensor stays in place for several days to a week and then is
replaced. A transmitter sends information about glucose levels via radio waves from the sensor to a
pager-like wireless monitor. The user must check blood samples with a glucose meter to program the
devices. Because currently approved continuous blood glucose monitoring devices are not as accurate
and reliable as standard blood glucose meters, they must be calibrated frequently during the course of
the day. They should not be used as a replacement for finger stick blood glucose or used in determining
insulin doses. It is essential that the patient receive education about calibrating the device and
interpreting the results.
Continuous blood glucose monitoring devices provide real-time measurements of glucose levels, with
levels displayed at 5-minute or 1-minute intervals. Users can set alarms to alert them when glucose
levels are too low or too high. Special software is available to download data from the devices to a
computer for tracking and analysis of patterns and trends, and the systems can display trend graphs on
the monitor screen. This can provide important information about patterns and trends so that patients
can make sense of what is affecting their blood glucose levels. Continuous blood glucose monitoring
provides a particular benefit for patients who experience erratic and unpredictable blood glucose drops,
as the alarm can alert them to take action before blood glucose drops to dangerous levels.
Hemoglobin A1c Monitoring
Hemoglobin A1c results should be obtained at least twice a year for patients with diabetes and every 3
months if glycemic targets have not been met or if there are treatment changes.
Complications
There are many complications related to both type 1 and type 2 DM. The various complications of longterm hyperglycemia are discussed later in the chapter. The focus here is on acute complications
including diabetic ketoacidosis(DKA), hypoglycemia, the dawn phenomenon, and the Somogyi effect.
Diabetic Ketoacidosis
In diabetes ketoacidosis, there is inadequate insulin for cells to obtain adequate glucose for normal
metabolism. The body attempts to obtain energy by the rapid breakdown of fat stores, releasing fatty
acids from adipose tissues. The liver converts the fatty acids into ketone bodies, which can serve as an
energy source in the absence of glucose. The ketone bodies, however, have a low pH, resulting in a
metabolic acidosis. The absence of insulin also results in an increased release of hormones such as
glucagon and cortisol in response to inadequate glucose transport into the cells. This leads to
gluconeogenesis and glycogenolysis, resulting in severe hyperglycemia resulting in hyperosmolality and
osmotic diuresis as discussed previously.
The causes of DKA include:
• Missed doses of insulin
• Inadequate insulin due to increased insulin needs secondary to stress or infection
• New diagnosis of type 1 diabetes
Clinical Manifestations. Similar to the initial presentation of DM, the initial patient presentation of DKA
is one of polyuria, polydipsia, and polyphagia. The patient becomes dehydrated, and electrolyte
imbalance such as hyperkalemia or hypokalemia may result (see Safety Alert). The increased serum
osmolality also results in a shift of fluid from the intracellular to the extracellular space, causing a
dilutional hyponatremia. The patient is also at risk for hypovolemia secondary to the osmotic diuresis.
Without treatment, the patient abruptly becomes hypotensive and tachycardic because of the volume
loss. The patient also develops Kussmaul’s respirations, which are rapid deep respirations that occur as a
compensatory mechanism for the acidosis. There is a fruity, acetone smell to the breath because of the
ketone bodies. The patient may complain of nausea and vomiting. Lethargy and coma may ensue
without prompt treatment. Figure 44.7 shows the common presenting clinical manifestations of DKA.
Diagnosis.
Diagnosis of DKA is based on several factors:
• Blood glucose level greater than 250 mg/dL
• Ketonuria (ketones in the urine)
• Arterial pH less than 7.30
• Serum bicarbonate level less than 18 mEq/L
• Positive anion gap
Anion Gap
Cations are positively charged ions. The major cations are sodium, potassium, calcium, and magnesium.
Anions are negatively charged ions: bicarbonate, chloride, phosphate, and albumin. The anion gap
provides an estimation of unmeasured anions in the blood. It is useful in determining the cause of
metabolic acidosis. It can also be used as a way of monitoring response to therapy. The premise of this
laboratory analysis is based on the need for electroneutrality in the body; the net positive charge must
equal the net negative charge.
The anion gap is calculated using three laboratory values: positively charged sodium, negatively charged
chloride, and negatively charged HCO3. Positively charged potassium is sometimes added to the
calculation, but typically the formula is as follows:
Anion gap = Na+ – (Cl- + HCO3-)
Serum sodium represents approximately 90% of the extracellular cations. Chloride and HCO3 represent
approximately 85% of the extracellular anions. Because of this, the normal anion gap—normal amounts
of unmeasured anions—is positive because the sum of the measured serum anions is smaller than the
sum of the measured serum cations or sodium in the formula. The normal value of the anion gap is 12
+/– 4.
If there is an addition of a positively charged acid, the anion gap will be altered. Diabetic ketoacidosis
results in an elevated anion gap as a result of the accumulation of acids in the serum. Response to
treatment can be monitored through evaluation of the anion gap. As the patient improves, the gap
should return to normal.
Treatment. Treatment priorities include:
• Fluid replacement with isotonic normal saline
• Insulin administration
• Correction of electrolyte imbalances
Fluid replacement with isotonic normal saline is essential to reverse the dehydration that has resulted
from the osmotic diuresis. Insulin administration is necessary to correct the hyperglycemia. Monitoring
and correcting electrolyte imbalances is essential to avoid dysrhythmias or neurological complications
that can occur with potassium and sodium imbalances.
Safety Alert
Monitoring and correcting potassium imbalances are essential in the treatment of DKA. Initially,
hyperkalemia may be present because of the movement of positively charged potassium ions out of the
cell in an effort to maintain homeostasis as positively charged hydrogen ions move into the cell as they
accumulate in the extracellular fluid. Hypokalemia then ensues as a result of the loss of extracellular
potassium in the urine because of the osmotic diuresis. This results in a severe total body loss of
potassium, making the patient susceptible to lethal arrhythmias. Care must be taken to monitor
potassium levels prior to treating the hyperglycemia with insulin. As insulin is administered to decrease
hyperglycemia, potassium will also move back into the cell, worsening hypokalemia. If hypokalemia is
present, potassium replacement is a priority.
Hypoglycemia
Hypoglycemia is an important and dangerous complication of the treatment of diabetes. It can present
as an acute or even life-threatening emergency due to the potentially devastating effects on the central
nervous system. Unlike other tissues of the body that can utilize fatty acids for energy needs, the central
nervous system relies solely on glucose for its energy needs. It needs a constant supply to maintain
metabolic functioning and avoid cell death.
Hypoglycemia, defined as a blood glucose level of less than 65 mg/dL, results when there is more
circulating insulin than is needed to handle the amount of circulating glucose. Surplus insulin can be the
result of an overly high dose of insulin administered, overly high dose of the oral agents that stimulate
insulin release, or reduced clearance of insulin from the body because of renal insufficiency. Patients are
at risk for hypoglycemia when they have a decreased nutritional intake or increased metabolism of
glucose through increased exercise. Alcohol can also reduce blood glucose levels by blunting the release
of glucose from the liver. Hypoglycemia is more severe when the early signs of low blood glucose are
blunted, as in the elderly or those who have a change in mental status.
Clinical Manifestations. When blood glucose levels drop below normal levels, the body attempts to
raise glucose through the stimulation of the sympathetic nervous system and release of hormones such
as epinephrine, norepinephrine, and glucagon. Symptoms include:
• Anxiety
• Hunger
• Palpitations
• Paresthesia (numbness at lips)
• Sweating
• Shakiness
If blood glucose levels continue to drop, reaching levels where the central nervous system is
inadequately supplied with glucose, symptoms include:
• Difficulty thinking
• Dizziness
• Fatigue
• Sleepiness
• Slurred speech
• Weakness/Lack of coordination
If untreated and hypoglycemia progresses further, these symptoms can progress to:
• Seizures
• Coma
If hypoglycemia occurs frequently, the body can lose the early warning signals of sympathetic nervous
symptoms. If patients have the accompanying “hypoglycemia unawareness,” they will not experience
symptoms of low blood glucose until their blood glucose levels fall to the point where the patients are at
risk for neurological symptoms. They are then at risk of severe effects such as confusion or loss of
consciousness. Individuals with hypoglycemia unawareness should be advised to raise their glycemic
targets to strictly avoid further hypoglycemia for at least several weeks to partially reverse hypoglycemia
unawareness and reduce risk of further episodes.
Management of Hypoglycemia. The primary management technique consists of the administration of
glucose to raise serum glucose levels. Oral glucose (15–20 g) administration is the preferred treatment
for the conscious individual with hypoglycemia, although any form of carbohydrate that contains
glucose may be used. Juice, soda, bread, or crackers work well. Carbohydrates that contain fat, such as
ice cream, are not recommended. Pure glucose is the preferred treatment because fat may retard
glucose absorption, prolonging the acute hypoglycemic event. After ingestion of carbohydrate,
monitoring of blood glucose levels should be measured within 15 minutes. If blood glucose levels
continue to reflect hypoglycemia after treatment, the treatment should be repeated. Once glucose
levels return to normal, the individual should consume a meal or snack to prevent recurrence of
hypoglycemia.
In the hospital setting, if a patient is unable to swallow or absorb oral carbohydrates but has IV access,
IV dextrose, 25 to 50 mL of 50% dextrose solution (D50), should be administered. If there is no IV access
and the patient is unable to swallow or absorb oral carbohydrates, 1 mg of intramuscular glucagon
injection should be administered. Glucagon mobilizes glucose release from stores in the liver.
Glucagon administration is not limited to health-care professionals. Severe hypoglycemia, where the
individual requires assistance from another person and cannot be treated with oral carbohydrates
because of confusion or unconsciousness, should be treated with glucagon. It should be prescribed for
all individuals at risk of severe hypoglycemia, and caregivers or family members should be instructed in
its administration.
Dawn Phenomenon and Somogyi Effect
The dawn phenomenon and Somogyi effect are two other complications of DM that result in increased
blood glucose levels in the early morning. They occur more commonly in the patient with type 1
diabetes, but are also known to occur in patients with type 2 diabetes. The increased blood glucose
levels of the dawn phenomenon result from the naturally occurring release of hormones such as
glucagon, cortisol, and growth hormone in the early morning. Because the body does not have sufficient
insulin to control this glucose surge, blood glucose levels rise. This is most likely reflected in higher
fasting blood glucose levels in the morning.
The Somogyi effect results in increased blood glucose levels due to an excessive insulin dosage at night.
This can occur in a patient who injects basal insulin before bed without also having a small bedtime
snack. In that circumstance, blood glucose levels drop and the body responds in the same way as in the
dawn phenomenon, releasing growth hormone, cortisol, and catecholamines in an effort to increase
blood glucose by releasing glucose stores from the liver. As stated, both complications result in higher
than normal blood glucose levels in the morning.
In order to determine what is causing the increased blood glucose levels in the morning, the patient
needs to check blood glucose levels in the early morning hours, 2 or 3 a.m., for several nights. If the
blood glucose level is low at that early morning time, the high glucose levels later in the morning are
most likely due to the Somogyi effect. If the blood glucose level is high or normal at that early morning
hour, the increased levels later in the morning are most likely due to the dawn phenomenon.
Nursing Interventions
■ Assessments
• Vital signs
Decreased blood pressure and increased heart rate are secondary to fluid volume deficit created by the
osmotic diuresis related to hyperglycemia. Increased respiratory rate, Kussmaul’s breathing or
hyperventilation with fruity breath odor, may be evident in DKA in an effort to compensate for the
metabolic acidosis.
• Intake and output
Increased urine output may be present because of osmotic diuresis secondary to hyperglycemia.
• Serum glucose
Increased glucose levels are due to the lack of secretion of insulin from the pancreas. In a patient already
diagnosed with and being treated for type 1 diabetes, increased glucose levels indicate:
• Inadequate or lack of insulin administration
• Increased insulin requirements due to stress such as infection causing adrenal release of
catecholamines, increasing the hepatic production of glucose
Decreased glucose levels caused by inappropriate insulin administration, such as too much insulin or
insulin given while the patient has inadequate PO intake, can lead to lethargy and coma or death. The
brain uses only glucose for cellular metabolism, so it is severely affected by decreased glucose levels.
• Potassium levels
Potassium levels may be decreased because of the increased volume loss through the kidneys or
increased because of the shift of the positively charged potassium out of the cell in an effort to maintain
homeostasis when positively charged hydrogen ions move into the cell in the face of acidosis.
• Carbohydrate intake at meals
Adequate carbohydrate intake at meals is essential to avoid hypoglycemia related to insulin
administration.
■ Actions
• Bedside glucose monitoring (finger sticks) done before meals and at bedtime
Regular finger sticks are done to measure the adequacy of glucose control.
• Administer insulin as ordered
• Basal
• Preprandial
• Correctional
Administering rapid-acting insulin before meals, preparing for ingestion of carbohydrates and
correcting for random high glucose levels as determined by self-monitoring of blood glucose prior to the
meal, in combination with longer-acting insulin once a day mimics the action of a healthy pancreas,
helping to maintain tight glycemic control. In patients with questionable or minimal oral intake, prandial
and correctional insulins may be administered together after meals after adequate carbohydrate intake
has been confirmed.
• Administration of isotonic IV fluids as ordered
IV fluids may be necessary to replace volume lost as a result of osmotic diuresis.
■ Teaching
• Subcutaneous insulin administration:
• Common sites that provide good absorption (starting with the area of best absorption) include the
abdomen, upper arm, thigh, and buttocks.
• Rotating sites
Insulin is administered subcutaneously. It is a protein substance. If taken orally, it is broken down in the
gastrointestinal tract rendering it useless. Rotating sites helps decrease lipohypertrophy (fat deposits in
the skin) or lipoatrophy (loss of fatty tissue). Rotating sites within one area rather than moving from area
to area helps decrease absorption variability from day to day. This can be done by injecting a new shot at
least an inch away from the last injection site (Figure 44.8).
• Subcutaneous injection technique
To ensure injection into the subcutaneous tissue, pinch the skin at the injection site and insert the needle
straight in at a 90° angle. If the patient is very thin with very small amounts of subcutaneous tissue, the
needle should be inserted at a 45° angle
• Syringe size
Choose the syringe size (1 mL, 0.5 mL, 0.3 mL) that best matches your insulin dose. The smaller syringes
allow for more accurate measurement of smaller insulin dosages.
• Infection control
Immediately discard used syringes and needles; use a new needle for each dose.
• Medication education
Lifelong insulin administration is required for cellular metabolism. Increased stress, infection, activity
level, increased ingestion of carbohydrates, and decreased PO intake all alter insulin requirements.
• Regular blood glucose monitoring via finger sticks
Regular checks help determine the adequacy of insulin dosage and maintain glycemic targets.
• Healthy lifestyle that includes diet and exercise (see section later in chapter on diet and exercise)
Healthy lifestyle choices are essential components in the management of DM to help avoid or postpone
the development of complications.
• Signs of hypoglycemia and hyperglycemia
It is important that the patient (and family) is able to detect early signs of both hypoglycemia (the
underlying disorder that can progress to coma or death) and hyperglycemia secondary to inadequate
insulin administration.
Evaluating Care Outcomes
The patient with type 1 DM can lead a long and healthy life with strict adherence to the treatment
regimen. The tight glycemic control necessary to avoid the complications associated with DM is best
achieved through active monitoring of blood glucose levels and treatment with insulin as indicated.
Nutrition, patient education, self-management, and detection and prevention of complications are
essential components of successful daily management of DM.