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Type 1 Diabetes
Jessica Lucier; Priyanka M. Mathias.
Last Update: October 5, 2024.
Continuing Education Activity
Type 1 diabetes is a disease involving the immune-mediated destruction of insulin-producing
pancreatic β-cells, leading to insulin deficiency. Type 1 diabetes is less common in adults than in
younger individuals and should be distinguished from type 2 diabetes, which is more prevalent in
older populations. Individuals with type 1 diabetes require lifelong exogenous insulin
replacement. Without insulin, patients can develop severe hyperglycemia and, ultimately,
diabetic ketoacidosis, which can be life-threatening. Besides insulin therapy, glucose monitoring,
disease-specific education, diet, and lifestyle modifications are cornerstones of type 1 diabetes
management. Diabetes self-management education and support should include training on blood
glucose monitoring, insulin administration, ketone testing when indicated, nutrition education,
methods to avoid and treat hypoglycemia, and sick day rules.
This activity for healthcare professionals is designed to enhance learners' proficiency in
evaluating and managing type 1 diabetes. Participants gain a broader grasp of the
condition's epidemiology, etiology, potential complications, and evidence-based diagnostic and
therapeutic strategies. Greater competence enables clinicians to collaborate effectively within an
interprofessional team caring for patients with type 1 diabetes, improving outcomes.
Objectives:
Identify the pathophysiological mechanisms underlying type 1 diabetes, including the role
of autoimmune processes and genetic factors, to better inform diagnosis and treatment
strategies.
Implement the latest advancements in diabetes technology to optimize glycemic control.
Differentiate between type 1 and type 2 diabetes, especially in adults, to guide appropriate
treatment strategies.
Implement effective collaboration and communication among interprofessional team
members to improve outcomes and treatment efficacy for patients with type 1 diabetes.
Access free multiple choice questions on this topic.
Introduction
Type 1 diabetes (T1D) is a condition characterized by the immune-mediated destruction of
insulin-producing pancreatic β-cells, leading to absolute insulin deficiency. The metabolic,
genetic, and immunogenetic characteristics of T1D are heterogeneous, with age-related
differences necessitating a personalized approach for each individual. Underlying genetic risk is
present in many individuals with the disease. Hence, the American Diabetes Association (ADA)
recommends that first- and second-degree relatives of individuals with T1D be screened and
offered T1D autoantibody testing.[1]
Individuals with multiple T1D-related autoantibodies eventually develop clinical disease. The
loss of insulin secretion can occur gradually or rapidly. Classic symptoms at the onset include
polyuria, polydipsia, and unintentional weight loss, but the clinical presentation varies
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individually. Adults with new-onset T1D usually present with symptoms similar to those seen in
children but may have a more gradual progression.
Diabetic ketoacidosis is more prevalent among young patients with new-onset T1D.[2] Disease-
modifying therapy has now been approved in the early preclinical stages of T1D to delay the
onset of clinical diabetes.[3] Other immune-modifying therapies to delay disease onset in at-risk
patients are also being studied.
Successful T1D management requires an interprofessional approach to patient care. Besides
insulin replacement therapy, diabetes self-management education, nutrition support, and
effectively recognizing and managing coexisting psychological issues are essential for
optimizing T1D outcomes. A collaborative, interprofessional approach is
recommended, involving many healthcare professionals, including nurses, dietitian educators,
pharmacists, community resources, and specialists as needed, such as podiatrists, mental health
professionals, social workers, ophthalmologists, and cardiologists.[4]
Etiology
T1D results from the autoimmune destruction of the β-cells in Langerhans pancreatic islets,
ultimately leading to absolute insulin deficiency.[5] This disease manifests in genetically
susceptible individuals in whom the autoimmune process is triggered by one or more
environmental factors, resulting in immune-mediated β-cell destruction. The loss of β-cell
function progresses gradually over months to years, during which time the affected individual
remains asymptomatic. Symptomatic hyperglycemia develops when a significant amount of β-
cell dysfunction occurs.
Genetic Associations of Type 1 Diabetes
The exact etiology of T1D remains unknown. However, a genetic predisposition is strongly
associated with specific human leukocyte antigen (HLA) alleles DR and DQ. HLA genes have
been reported to account for approximately 40% of the familial aggregation of T1D. The HLA
class II DRB1, -DQA1, -DQB1 genotypes confer the strongest genetic risk factors for T1D.
[6] Specifically, HLA DR4-DQ8 and DR3-DQ2 have been reported to be present in about 90% of
children with T1D.
The lifetime risk of developing T1D is significantly increased in close relatives of a patient with
T1D. However, most cases occur in patients without any family history of T1D or other
autoimmune disease. This association is more pronounced in youth-onset than adult-onset T1D.
[7] Multiple other genes also contribute to heritability.[8] Screening of family members must be
considered, especially first-degree relatives of individuals with T1D, to identify people who may
be at risk.
Environmental Risk Factors
Environmental factors are generally believed to trigger autoimmune β-cell destruction in
genetically susceptible people. Some studies have found an increased T1D risk related to
infection with Coxsackie virus, enteroviruses, cytomegalovirus, rubella virus, influenza B,
mumps virus, and more recently, SARS-CoV-2 (COVID-19).[9][10][11] Other environmental
factors that may increase risk include pregnancy and perinatal conditions, childhood vaccination,
and dietary factors such as cow's milk and cereal exposure. Research to better understand the
exact role of these environmental agents in the etiology of T1D is ongoing.
Autoimmunity
Besides genetic and environmental factors, several T1D-related autoantibodies target pancreatic
β-cell autoantigens, leading to immune-mediated β-cell destruction. Autoantibody targets include
antigens in the islet cell cytoplasm (ICA), insulin (IAA), glutamic acid decarboxylase isoform 65
(GAD65), insulinoma antigen 2/islet tyrosine phosphatase 2 (IA-2), and zinc transporter isoform
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8 (ZnT8). IAAs are primarily detected in children.[12] GAD65 is the most common autoantibody
detected in adults.[13] Testing for autoantibodies to pancreatic β-cell autoantigens is important in
confirming the diagnosis and distinguishing T1D from other forms of diabetes, mainly type 2
diabetes (T2D). The greater the number of detectable antibodies and the higher their titers, the
greater the risk of developing T1D.
Epidemiology
T1D is one of the most frequent chronic diseases in children, but the disease can affect any age
group. Childhood-onset T1D tends to present with more severe clinical presentations, including
symptomatic severe hyperglycemia or diabetic ketoacidosis (DKA). In adults, new-onset
T1D may be misdiagnosed as T2D, but youth-onset T1D is more common than adult-onset
T1D. Although autoimmune disease tends to be more commonly seen in women, T1D appears to
be slightly more common in men.[14]
T1D incidence and prevalence have steadily increased, now representing approximately 5% to
10% of people with diabetes. A systematic review and meta-analysis reported that the worldwide
prevalence of T1D was 9.5%, with an incidence of 15 per 100,000 people.[15] Worldwide, T1D's
geographic incidence varies considerably. The highest reported incidences are in Finland and
other Northern European nations, with rates approximately 400 times greater than those seen in
China and Venezuela, where incidence is reportedly the lowest.
Pathophysiology
The natural history and development of T1D in genetically susceptible individuals occur in 3
stages. Stage 1, the preclinical stage, is characterized by the onset of autoimmune β-cell
destruction and insulitis caused by immune-mediated destruction. This stage is asymptomatic and
characterized by normal fasting glucose, normal glucose tolerance, and the presence of at least 2
pancreatic autoantibodies. In Stage 2, a significant amount of β-cell dysfunction has already
occurred, leading to dysglycemia. The diagnostic criteria include the presence of pancreatic
autoantibodies with impaired fasting glucose (fasting glucose 100-125 mg/dL), impaired glucose
tolerance (2-hour post-75 g glucose load glucose 140-199 mg/dL), or a glycated hemoglobin
(HbA1c) level of 5.7% to 6.4%. Individuals remain asymptomatic.
Stage 3 is characterized by the clinical onset of disease where individuals present with
symptomatic hyperglycemia. The diagnostic criteria include diabetes, defined by hyperglycemia
(random glucose ≥200 mg/dL) with clinical symptoms, fasting glucose of at least 126 mg/dL,
blood glucose level of at least 200 mg/dL 2 hours after ingesting 75 g of glucose during an oral
glucose tolerance test, or HbA1c greater than or equal to 6.5%. T1D classically presents with
symptomatic hyperglycemia, especially in children. Individuals with classic new-onset T1D
usually present with symptoms of polydipsia, polyuria, polyphagia, unintentional weight loss,
fatigue, and weakness. Life-threatening DKA can develop if T1D is not evaluated and treated
promptly.
DKA is characterized by hyperglycemia, ketonuria, and electrolyte disturbances that lead to
metabolic acidosis. Besides polyuria, polydipsia, and unintentional weight loss, patients in DKA
may present with fruity-smelling breath, lethargy, and, in severe cases, even coma. Early
detection and initiation of treatment, including intravenous fluids, insulin, potassium, and careful
monitoring, is important. Most patients require admission to an intensive care unit for
management and monitoring. The incidence of DKA in children ranges anywhere between
15% and 70%.[16]
The onset of symptoms in adults is more variable than in younger patients, and DKA is less
common. Patients are often misdiagnosed with T2D and later found to be insulin-dependent.
T1D can be difficult to distinguish from T2D. Screening for T1D antibodies and family history
are important in confirming the diagnosis.
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GAD65 should be the initial antibody tested when T1D in adults is suspected. IA2 or ZNT8
should be measured if GAD65 testing is negative or unavailable. C-peptide levels may also be
used to determine β-cell function and the degree of insulin dependency when the diagnosis is still
unclear. In patients with T1D, fasting insulin and C-peptide levels are inappropriately low when
the concomitant plasma glucose concentration is elevated. By contrast, elevated fasting insulin
and C-peptide levels suggest T2DM.
History and Physical
After the initial diagnosis and medical stabilization, successful management of T1D involves
improving glycemic control, preventing long-term complications and sequelae of hyperglycemia,
and T1D education while maintaining normal growth and development in children and
improving quality of life. Initial diabetes education provided by an interprofessional care team is
essential for the patient and family to acquire the knowledge needed to manage this chronic
disease. Clinicians need to reinforce that multiple factors impact glycemic control and involve
the patient or family in a comprehensive treatment plan that emphasizes a healthy lifestyle,
which can improve disease outcomes.
At the initial outpatient visit, obtaining a complete medical, psychosocial, and family history,
including pregnancy and contraception history, is essential. History of prior diabetes education,
monitoring of blood glucose and ketones, administration of insulin, and recognition and
treatment of hypoglycemia should be obtained. Particular attention should be paid to the date of
diagnosis, prior treatment received, knowledge of sick day rules, and history of acute
complications (severe hypoglycemia or DKA) and chronic complications (eg, skin disorders,
dental problems, diabetic retinopathy, diabetic neuropathy, kidney disease, cardiovascular
disease, peripheral arterial disease, stroke, foot ulcers, and foot amputations).
Since people with T1D have an increased risk of developing other autoimmune disorders,
including autoimmune thyroid pathology and celiac disease, the clinician should also screen for
these conditions during clinical evaluation. Several measures are available for psychosocial
screening, such as the Patient Health Questionnaire (PHQ-2/PHQ-9) for Depression and
Generalized Anxiety Disorder (GAD-7). Diabetes distress and social determinants of health
should be assessed. Eating disorders are common in individuals with type 1 diabetes, particularly
young women. Thus, patients should be examined for this problem. Early cognitive decline is
also common in adults. Therefore, cognitive testing should be considered when impairment is
suspected.
A complete physical examination is also performed. A diabetes foot examination must be
included to detect early peripheral neuropathy signs, foot deformities, pre-ulcerative lesions,
ulcerations, calluses, and onychomycosis. Testing vibratory and protective sensations is also
essential. Abnormal testing with a 10-g monofilament exam suggests an increased risk of
ulceration. The skin should be examined, especially at insulin injection or infusion sites. If
lipodystrophy is evident, patients should be educated on the importance of varying insulin
injections or infusion sites.
Evaluation
Patients with T1D can present with classic symptoms of new-onset diabetes, such as polyuria,
polydipsia, lethargy, and weight loss. These individuals may also present more acutely with
DKA. Other clinical manifestations include acute visual disturbances, perineal candidiasis, or, in
some adults, an initial misdiagnosis of T2D before correctly identifying T1D.
Diabetes may be diagnosed using plasma glucose criteria, such as fasting plasma glucose or
postprandial glucose during a 75-g oral glucose tolerance test (OGTT), or based on HbA1c
levels. Diagnostic criteria for diabetes include the following:
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Fasting plasma glucose of at least 126 mg/dL on more than 1 occasion
Random plasma glucose of at least 200 mg/dL with classic symptoms of hyperglycemia
Plasma glucose of at least 200 mg/dL measured 2 hours after a 75-g OGTT
HbA1C level of at least 6.5%[17]
In the absence of unequivocal hyperglycemia, the diagnosis is confirmed based on 2 abnormal
test results. Once the diagnosis of diabetes is confirmed, distinguishing between T1D and other
forms of diabetes, mainly T2D, is critical. These conditions may be differentiated based
on clinical presentation and laboratory studies, including testing for T1D pancreatic
autoantibodies and stimulated C-peptide levels, with the latter measuring pancreatic β-cell
function. T1D pancreatic antibodies include ICA, IAA, GAD65, IA-2, and ZnT8. Most patients
with T1D have 1 or more positive T1D antibodies at the time of diagnosis.
Evaluating glycemic control by checking HbA1c levels is recommended every 3 months during
each follow-up visit. Other laboratory tests that should be conducted, if not performed within the
past year, include a lipid profile, serum creatinine, spot urinary albumin-to-creatinine ratio, liver
function tests, thyroid-stimulating hormone, complete blood count with platelets, and serum
potassium—especially if the patient is also taking an angiotensin-converting enzyme inhibitor,
angiotensin receptor blocker, or diuretic. Since people with T1D are at an increased risk of
developing other autoimmune diseases, such as autoimmune thyroid conditions, celiac disease,
primary adrenal insufficiency, and rheumatoid arthritis, screening for autoimmune disorders
should be considered when clinically appropriate.[18]
Treatment / Management
Individuals with T1D require lifelong insulin replacement, regular blood glucose monitoring, and
adjustments in diet and lifestyle to achieve optimal glycemic control. Glycemic targets should be
personalized based on each patient's health status and coexisting conditions, guiding treatment
strategies. According to the ADA, optimal HbA1c levels should be reached to minimize the risk
of microvascular and macrovascular complications while preventing hypoglycemia. For most
patients, an HbA1c goal of less than or equal to 7% is recommended, though older individuals or
those with multiple health issues may benefit from more relaxed HbA1c targets.
Insulin Replacement
The goal in T1D management is physiologic replacement of insulin, either by administering
multiple daily insulin injections (MDI) or continuous subcutaneous insulin infusion via an
insulin pump. MDI or "basal-bolus" insulin therapy includes basal long-acting insulin
(administered once or twice a day) and prandial or mealtime insulin using short-acting or rapid-
acting insulin multiple times a day before meals. Continuous subcutaneous insulin infusion
includes administering a rapid- or short-acting insulin continuously via an insulin pump with
additional boluses initiated on the pump for prandial coverage at mealtimes.
Multiple daily injections
Various insulin types may be used for insulin injection therapy.[19] The choice of basal and
prandial insulin for MDI usually depends on patient preference, insurance coverage, availability,
and cost. Long-acting insulin is preferred for basal insulin injection therapy, often given once a
day (U-100 and U-300 glargine, degludec) or 1 to 2 times daily (detemir and U-100 glargine).
Glargine does not have a pronounced peak and lasts approximately 20 to 24 hours. U-300
glargine lasts more than 24 hours, and degludec has a longer duration of action, up to 42 hours.
Intermediate insulin, eg, neutral protamine Hagedorn or neutral protamine lispro, is the least
expensive basal insulin but is more likely to cause hypoglycemia. Intermediate insulin's action
onset is 1 to 2 hours. Peak action is at 2 to 8 hours, and duration is 12 to 24 hours. This insulin
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form is usually given before breakfast and bedtime. When MDI is used, the patient
should inject rapid-acting insulin with each meal for hyperglycemia correction and a daily long-
acting basal insulin.
For prandial or mealtime coverage, options include rapid-acting insulin, ultra-rapid-acting
insulin, and short-acting regular insulin. This type of insulin is usually administered within 10 to
15 minutes before meals. Rapid-acting insulin (lispro, aspart, glulisine) generally has an onset of
12 to 30 minutes, peaks in 1 to 3 hours, and has a duration of action of 3 to 6 hours. Ultra-rapid-
acting lispro or aspart has a slightly quicker onset and somewhat shorter duration. Short-acting
insulin (regular insulin) has an onset of 30 minutes to 1 hour, peaks in 2 to 4 hours, and has a
duration of 5 to 8 hours. MDI regimens must be titrated to target a blood glucose range of,
usually, 79 to 180 mg/dL while minimizing the risk of hypoglycemia (<70 mg/dL) and
hyperglycemia (>180 mg/dL).
Continuous subcutaneous insulin infusion
Continuous subcutaneous insulin infusion (CSII) or insulin pump therapy administers a
continuous infusion of insulin, usually a rapid-acting insulin, to replace the basal insulin
requirement. Besides basal insulin, mealtime insulin boluses are administered via the pump for
prandial coverage. The insulin pump consists of the pump itself, a reservoir or cannula for
holding insulin, insulin tubing, and a cannula or needle inserted subcutaneously. Advances in
diabetes technology have led to newer insulin pumps that connect to continuous glucose
monitors (CGMs) and enable automated insulin delivery to target optimal glycemic control.
Several types of insulin pumps are available. Sensor-augmented insulin pumps function
independently from CGMs. Predictive low-glucose suspend insulin pumps are programmed to
halt insulin delivery when blood glucose drops to a prespecified low threshold. Automated
insulin delivery or hybrid closed-loop systems integrate an insulin pump with a connected CGM
to automatically adjust insulin delivery based on CGM values and maintain blood glucose within
the target range. Do-it-yourself automated insulin delivery systems are also known as "looping."
Blood Glucose Monitoring
Monitoring blood glucose is an integral part of T1D management. Monitoring can
be accomplished through capillary blood sampling with a glucose meter or CGM systems that
provide real-time glucose data via a sensor and reader or smartphone app.
Glucose meter
Patients using a blood glucose meter should check their blood sugar levels at least 4 times a day,
including before meals and at bedtime. Numerous blood glucose meters are available on the
market, and the choice of meter often depends on cost or insurance coverage.
Continuous glucose monitors
CGMs have now become the standard of care in diabetes management. These devices are
especially important in T1D management, as patients have an increased risk of frequent and
severe hypoglycemia and hypoglycemia unawareness. Real-time CGM devices measure glucose
every few minutes and automatically transmit glucose data to a receiver or phone application
device. The device can also alarm when hypoglycemia or hyperglycemia triggers are met. CGMs
collect real-time blood glucose data and trends, allowing patients to anticipate blood glucose
levels for the next 30 to 60 minutes and adjust treatment decisions accordingly. Intermittent or
flash-type glucose monitoring devices are also available. These devices require patients to
periodically scan their sensors with a reader or phone application to obtain blood glucose
readings.
Diabetes Education and Self-Management
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Optimal T1D management includes intensive education on diet, lifestyle, insulin management,
and blood glucose monitoring. Treatment regimens and goals are often complex, requiring
patients to receive ongoing education and self-management support to achieve these goals.
Patients must understand the interaction between insulin, diet, physical activity, and daily
activities on their blood glucose levels. They also need to appreciate the importance of adhering
to their insulin regimen and monitoring blood glucose. Education should also cover ketone
monitoring, sick day rules, detection and early treatment of hypoglycemia, and screening for
diabetes complications. When appropriate, the patient’s family and caregivers should also be
educated to provide adequate support.
Nutrition education, including carbohydrate estimation and counting, is important in diabetes
management. Carbohydrate counting is often essential for patients to achieve optimal mealtime
blood glucose targets and to accurately estimate prandial insulin needs. Carbohydrate estimation
helps reduce the risk of hypoglycemia. For example, patients may have an increased risk of
postprandial hypoglycemia if they consume a low-carbohydrate meal but administer the full
amount of mealtime insulin without adjusting for the actual carbohydrate content. Patients should
consult with a dietitian when possible to learn carbohydrate counting and be instructed to use an
insulin-to-carbohydrate ratio (grams of carbohydrate covered by 1 unit of insulin) for mealtime
dosing. If carbohydrate counting is not feasible, maintaining a carbohydrate-consistent diet may
be the best alternative. Besides dietary education, incorporating physical activity is important for
people living with T1D. Physical activity is encouraged for its beneficial effects on insulin
sensitivity and overall health, but it requires careful management to avoid glucose fluctuations.
Hypoglycemia
Hypoglycemia is the most frequent adverse effect of insulin therapy. Educating people
living with T1D and their partners about the signs and symptoms of hypoglycemia is crucial.
Symptoms include sweating, rapid heartbeat, lightheadedness, confusion, hunger, visual changes,
and tremors. Symptoms of hypoglycemia typically occur when blood glucose levels drop below
70 mg/dL, known as level 1 hypoglycemia. Level 2 hypoglycemia occurs when blood glucose
levels fall below 54 mg/dL and is usually associated with cognitive impairment and altered
consciousness. Level 3 hypoglycemia involves a hypoglycemic episode that requires assistance
from another person for resuscitation.
Recurrent hypoglycemic episodes, particularly in individuals with a longer duration of T1D, can
lead to hypoglycemia unawareness. This condition occurs when individuals experience
hypoglycemia symptoms at progressively lower glucose thresholds, likely due to reduced
sympathoadrenal responses or autonomic failure. Hypoglycemia not only impacts the quality of
life in people living with T1D but also increases the risk of cardiovascular events and mortality.
In older adults or frail individuals, hypoglycemia can heighten the risk of falls, cognitive
impairment, dementia, and fractures.
Patients must be educated about the signs and symptoms of hypoglycemia, the blood glucose
thresholds for treatment, and the use of glucagon for severe hypoglycemia unresponsive to
conventional treatments. Individuals at risk for recurrent and severe hypoglycemia benefit from
using a CGM, which can alert them to treat hypoglycemia promptly. Hypoglycemia treatment
generally involves consuming 15 to 20 grams of glucose orally if blood glucose levels fall below
70 mg/dL. Blood glucose should be rechecked 15 minutes later, with additional
carbohydrates administered if necessary. Once blood glucose levels have normalized, a snack
should be provided to prevent recurrence. Glucagon should be prescribed for emergency use in
cases of severe hypoglycemia when the individual cannot consume carbohydrates orally.
Follow-up and Ongoing Care
Following the initial evaluation and diabetes visit, the diabetes care team should continue to
provide T1D education and support while assessing the patient's insulin regimen and blood
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glucose control. Regular visits with the endocrinologist, diabetes educator, nurse practitioner,
dietitian, and, if necessary, mental health professionals ensure comprehensive education and care
aimed at maintaining optimal glycemic control. At each follow-up visit, key aspects of glycemic
control, insulin management, the interaction between diet and exercise, and the treatment
regimen should be reinforced. The patient's blood glucose data, whether from a glucose
monitoring device or CGM, should be reviewed in detail with the patient.
For patients using an insulin pump or automated insulin delivery device, data from the device
should be downloaded and discussed when appropriate. Adjustments to the patient's treatment
regimen should be reviewed and reinforced as needed. Additionally, the clinician should screen
for diabetes complications and comorbidities at follow-up visits and arrange referrals to
specialists if necessary. Effective ongoing T1D management should also involve evaluating
overall health status and engaging in shared decision-making to set treatment goals.
Differential Diagnosis
T1D must be distinguished from similar conditions based on the patient's clinical presentation,
history, and laboratory studies. These conditions include type 2 diabetes, monogenic diabetes,
diseases affecting exocrine pancreas function (cystic fibrosis-related diabetes, chronic
pancreatitis0, posttransplantation diabetes mellitus, steroid-induced diabetes, and psychogenic
polydipsia.
Prognosis
T1D is a challenging condition to manage and can lead to complications that can shorten life
expectancy. However, morbidity and mortality associated with the disease have improved with
advances in insulin therapy and diabetes technology, improvement in glycemic control, and
control of metabolic risk factors such as hypertension and hyperlipidemia. Timely screening for
microvascular and macrovascular complications and strict glycemic control at disease onset have
reduced rates of serious diabetes-related complications. Mortality rates have declined, though
people with T1D have 2- to 5-fold higher mortality than those without diabetes. This issue is
discussed further in other sections.[20]
Complications
Complications secondary to T1D can be classified into acute and chronic conditions. Acute
complications include hypoglycemia and DKA. The most serious chronic complications include
nephropathy, peripheral and autonomic neuropathy, retinopathy, heart disease (including
coronary artery disease, heart failure, and cardiomyopathy), peripheral arterial disease,
cerebrovascular disease (including stroke and transient ischemic attack), and diabetic
foot infections.
Deterrence and Patient Education
Successful T1D management requires an interprofessional approach to patient care. Patient
medication compliance and follow-up with specialists and educators are critical factors in
preventing complications. At every patient encounter, the pharmacist, nurse, and clinician should
emphasize the importance of blood glucose control, screening for long-term complications, and
diabetes management goals. The patient should be encouraged to modify their lifestyle to reduce
the risk of complications. All individuals with diabetes should also be made aware of the signs
and symptoms of hypoglycemia and ways to prevent and treat this condition. Patients should be
educated about available resources and the benefits of joining diabetes support groups when
needed.
Enhancing Healthcare Team Outcomes
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Self-management of type 1 diabetes (T1D) involves MDI or insulin administration via an insulin
pump, along with glucose monitoring and careful attention to diet and physical activity. This
daily regimen can be burdensome and, in some individuals, eventually lead to diabetes distress or
burnout. While technological advancements have enabled better glycemic control, these
innovations often come with high costs, complexity, and the need for extensive education and
training. Additionally, many individuals with diabetes experience anxiety about hypoglycemia,
hyperglycemia, and potential complications, which can lead to mental health issues such as
depression, anxiety, and eating disorders.
Addressing the comprehensive medical, educational, psychological, and social challenges faced
by people living with T1D requires an interprofessional team approach. This team typically
includes primary care clinicians, endocrinologists, diabetes nurse educators, pharmacists,
dietitians, mental health professionals, social workers, podiatrists, and community resource
representatives. By adopting individualized treatment plans, which can lessen the burden of care
and further enhance outcomes, the interprofessional care model is positioned to achieve the best
possible patient results.
All members of the interprofessional team need to synchronize their efforts and maintain open
communication to ensure that all parties involved in patient care, including the patients
themselves, have access to accurate and updated information. Nurses are pivotal in coordinating
activities among various healthcare professionals and contribute significantly to patient
evaluation, education, and monitoring. Pharmacists, working closely with diabetes educators,
should ensure proper insulin dosing and participate in patient education and medication
reconciliation. These examples of interprofessional collaboration are key to driving improved
patient outcomes.
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Disclosure: Jessica Lucier declares no relevant financial relationships with ineligible companies.
Disclosure: Priyanka Mathias declares no relevant financial relationships with ineligible companies.
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