The goal of this program is to provide outpatient PTs with information about type 1 diabetes mellitus and how it might affect patients undergoing physical therapy. After reading this module, you will be able to —
Approval Information
Gannett Healthcare Group is an approved sponsor by the New York State Education Department of continuing education for physical therapists and physical therapist assistants from October 21, 2009 to October 21, 2012.
This activity is provided by the Texas Board of Physical Therapy Examiners Accredited Provider #GED012010TPTA2012004 and meets continuing competence requirements for physical therapist and physical therapist assistant licensure renewal in
As of 4/5/10, Gannett Education is recognized by the Physical Therapy Board of California as an approved reviewer and provider of continuing competency courses for the state of
Gannett Education was approved as a provider of continuing education by the North Carolina Physical Therapy Association (provider no. 09-0215-001PR) from March 8, 2009 through March 8, 2010.
The Illinois Chapter Continuing Education Committee has certified that this course meets the criteria for approval of Continuing Education offerings established by The Illinois Physical Therapy Association (approval no. 437.3060, expiration date 10/1/10). According to the Rules for the Administration of the Illinois Physical Therapy Act (section 1340.61) published by the Illinois Department of Professional Regulation, a physical therapist or physical therapist assistant applying for re-licensure in Illinois can earn a maximum of 50 percent of their required continuing education hours from self-study. The hours awarded of this course are designated for self-study CE credit.
Other states may accept this course for meeting their CE requirements. Check with your state association or board.
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Not all types of diabetes are created equal, and they vary in etiology, pharmacological management, musculoskeletal manifestations, nutritional goals, susceptibility for hypoglycemia, and responses to physical therapy treatment (outcomes). There seems to be a lack of regard in physical therapy documentation distinguishing type 1 and type 2 diabetes mellitus. The literature is lacking recommendations on specific components that should be included in the patient management model regarding patients with type 1 diabetes. Furthermore, there are other aspects in the care of patients with type 1 diabetes that clinicians may fail to address and that can predispose the patient to harm, such as the effect of exercise intensity on inducing hypoglycemia, management of hypoglycemia and hyperglycemia, and conditions under which a patient should not exercise. PTs may not be aware of the lesser-known complications directly caused by, or associated with diabetes, especially type 1 diabetes. Patients with diabetes may be referred for outpatient physical therapy for such conditions, but little emphasis or consideration may be given by clinicians regarding how poor glycemic control may manifest itself in these musculoskeletal disorders as this will alter expected outcomes and/or duration of treatment.
Disease Overview
Diabetes mellitus consists of a group of disorders characterized by impaired blood glucose mechanism, of which type 1 diabetes accounts for 5% to 10% of diagnosed cases.1 Patients with type 1 diabetes usually present with acute symptoms and markedly elevated blood glucose levels, requiring insulin for survival (as opposed to glycemic control as seen in type 2 diabetes). Type 1 diabetes occurs from pancreatic beta cell destruction due to an autoimmune response.2 Risk factors may be autoimmune, genetic, or environmental. The category terms of “insulin-dependent diabetes” and “non-insulin dependent diabetes” have changed to type 1 and type 2 diabetes, which more appropriately describe the epidemiology. It has been noted that the terms insulin-dependent diabetes and non-insulin dependent diabetes have been misunderstood and misused when classifying patients with diabetes as some people with type 2 diabetes may require insulin for management of the disease.3 Similarities and differences between type 1 diabetes and type 2 diabetes are listed in Table 1.
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Table 1: Type 1 Diabetes and Type 2 Diabetes at a Glance2 | ||
|
American Diabetes Association Standards of Medical Care in Diabetes—2009 |
Type 1 Diabetes |
Type 2 Diabetes |
|
Disease etiology |
Results from B-cell destruction leading to absolute insulin deficiency |
Result from a progressive insulin secretory defect on the background of insulin resistance |
|
Screening and testing for diagnosis |
Measurement of islet cell antibodies for high-risk individuals. |
Asymptomatic risk factors include BMI=25gk/m2, gestational diabetes, physical inactivity, family history of diabetes, dyslipidemia, hypertension, imparied glucose tolerance, history of CVD |
|
Glycemic pharmacologic management |
Intensive insulin therapy (three or more injections daily of insulin) with rapid and long-acting insulin analoges; or continuous subcutaneous insulin infusion (insulin pump therapy) with rapid-acting analog. |
Metformin at time of diagnosis, lifestyle changes (MNT and exercise), adding other oral agents and/or insulin as needed |
|
Self-monitoring of blood glucose recommendations |
=3 times daily for patients on multiple insulin injections of insulin pump therapy. Continuous glucose monitoring can be useful to lower A1C in adults (=25 years). |
For patients using less frequent injections, medical nutrition therapy, or noninsulin therapies, self-monitoring of blood glucose may be useful as guide on glycemic control |
|
HbA 1 c recommendations |
7%, less stringent in the presence of — · Frequent hypoglycemia · Advanced complications · Pregnancy · Children and adolescents |
7% |
|
Plasma glucose goals |
Preprandial: 70 to 130 mg/dl (3.9 to 7.2 mmo1/1) Peak postprandial: <180 mg/d1 (<10.0 mmo1/d1) Pregnancy: Before meals: =95 mg/d1 (5.3 mmo1/1) 1-h postmeal: =140 mg/d1 (7.8 mmo1/1) or 2-h postmeal: =120 mg/d1 (6.7 mmo1/1) |
Preprandial: 70 to 130 mg/dl (3.9 to 7.2 mmo1/1) Peak postprandial: <180 mg/dl (<10.0 mmo1/d1) |
|
Medical Nutrition Therapy |
Carbohydrate counting to reach glycemic goals. Follow recommended dietary allowance guidelines. No specific meal plan to follow other than encouraging a well-rounded diet. |
Weight loss is recommended, as this is one of the markers of type 2 diabetes and metabolic syndrome. Most studies on the role medical nutrition therapy and A 1 C have been done on type 2 diabetes. |
|
Physical activity |
At least 150 min/week of moderate-intensity aerobic exercise |
In addition to aerobic exercise, encouraged to perform |
Recently, there has been recognition of adults presenting with late-onset and slow progression of autoimmune diabetes and the terms “1.5 diabetes” and “latent diabetes of adults” (LADA) have been coined to describe this not-yet-officially-recognized sub-type of diabetes.4 Epidemiological data demonstrate that LADA accounts for about 10% of all cases of diabetes, making it as common as type 1 diabetes.5 Often, patients with LADA are diagnosed with type 2 diabetes because of the age at diagnosis (=30 years of age) and initial glycemic improvement with diet and oral agents, but they seem to more quickly progress to complete insulin deficiency. Patients with LADA share characteristics of both type 1 diabetes (positive antibodies6) and type 2 diabetes (although have fewer features of metabolic syndrome5). This sub-category of diabetes warrants mention because of similarities in management to type 1 diabetes. Due to the diagnostic confusion among patients with LADA, it may take longer for them to be effectively managed and expose them to hyperglycemia episodes that lead to complications despite the relative short time since diagnosis.
Medical history. More information is needed once the box indicating the patient has diabetes on the physical therapy intake sheet has been checked. Information regarding type and duration of diabetes, presence of diabetes complications, and management strategies used by the patient needs to be solicited and documented. Frequency of self-monitoring of blood glucose or the use of a continuous glucose sensor should be noted as well. The results of the Diabetes Control and Complications Trial,7 a landmark study, showed the positive effects of intensive insulin therapy, frequent glucose self-monitoring, and daily adjustments to food and insulin on lowering hemoglobin A1c (HbA1c) values and decreasing the risk of developing diabetes complications. An A1C (also known as glycated hemoglobin or HbA1c) blood test gives patients a picture of their average blood glucose control for the past two to three months. The amount of A1C in patients’ blood reflects blood sugar control for the past 120 days, or the lifespan of a red blood cell.
Patients should be re-evaluated periodically by their diabetes educator regarding the use of glucose self-monitoring to make adjustments to other disease management components. Patients who are less compliant with recommendations of monitoring their blood glucose may be unaware of hyperglycemia, hypoglycemia, and how to appropriately adjust insulin, food intake, and physical activity. Patient who perform more frequent glucose self-monitoring will have more information at their disposal to make changes in management, whereas the infrequent tester will not have as much information to impact self-management.
Insulin therapy. Based on the association between intensive management and lower risk of developing complications as found in the Diabetes Control and Complications Trial, the majority of type 1 diabetes patients are on multiple daily injections or insulin pump therapy.2,8 Intensive treatment consists of three or more injections daily or use of an insulin pump. With multiple-daily injections, patients inject either intermediate or long-acting insulin to cover the basal requirements of insulin and take rapid or short-acting insulin when food is eaten. Multiple daily injections require timing food intake and physical activity based on the timed actions of the injected insulin. Even with long-acting insulin there is variability of absorption that can impact glycemic control.
Insulin pumps9 are insulin delivery systems that use rapid or fast-acting insulin only. They deliver small amounts of insulin at a time, making delivery and absorption more consistent, which is more equivalent to the normal physiological delivery of insulin. Pumps are the size of a beeper or small cell phone, and they release insulin into the interstitial tissue via an infusion set, like an IV, which is changed every two to three days. Additional insulin is programmed by the patient to be delivered when meals are to be eaten, much like the pancreas would release extra insulin when food is present in the body. The types of delivery are termed basal bolus and meal bolus respectively. Since there are no peaks in insulin to contend with, patients choose when to eat and how much.10 In order to do this, an insulin-to-carbohydrate ratio needs to be determined so patients know how much rapid-acting insulin is needed to cover the carbohydrate eaten at a meal or snack. This is used as part of a more advanced level of carbohydrate counting. Table 2 lists the more commonly used recombinant-DNA insulin preparations used for multiple daily injections and pump therapy.11
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Table 2: Pharmacokinetics of Insulin Preparations Used in Type 1 Diabetes Management11 | ||||
|
Class |
Insulin type |
Onset |
Peak (h) |
Duration (h) |
|
Rapid acting |
Aspart (Novolin) Lispro (Humalog) Giulisine (Apidra) |
<15 min |
1 to 2 |
3 to 4 |
|
Short acting |
Regular (Novolin, Humulin) |
0.5 to 1 h |
2 to 3 |
3 to 6 |
|
Intermediate acting |
NPH (Humulin N) |
2 to 4 h |
4 to 10 |
10 to 16 |
|
Long acting |
Detemir (Levemir) Glargine (Lantus) |
2 to 4 h |
peakless |
24 |
Meal Planning. Carbohydrate counting is the meal-planning method commonly used by patients with type 1 diabetes to synchronize food choices with insulin to be delivered. Post-prandial (post-meal) blood glucose levels are used to modify the insulin-to-carbohydrate ratio. Unlike type 2 diabetics, who may have a weight loss goal as part of their medical nutrition therapy, patients with type 1 diabetes are only advised to maintain healthy eating habits2 and rely on carbohydrate counting alone to determine insulin dosing.12 One common misconception that many people, including PTs, have is that patients with type 1 diabetes need to follow a diabetic-diet or should avoid eating sugar. This is no longer true with type 1 diabetes; patients can partake of previously “forbidden foods” by using carbohydrate counting and becoming skilled at what effect those types of foods have on their blood glucose levels.13
Fats and protein have little effect on blood glucose levels unless consumed in large amounts, which can then reduce the absorption of carbohydrates. When eating fried or high-fat foods, patients may have elevated blood glucose levels four to six hours later, although their glucose levels were within target-range an hour or two after eating. Fiber recommendations are the same as for the general population and, due to the low glycemic index, have the added benefit of slowing down post-prandial rise in blood glucose.
Self-monitoring of blood glucose and continuous glucose monitoring. Frequent self-monitoring of blood glucose is crucial to patients with type 1 diabetes. Type 1 diabetics on multiple daily injections or pump therapy should carry out three or more glucose meter tests per day.2 With more intensive glycemic control, there may be higher incidence of hypoglycemic episodes, as found in the Diabetes Control and Complications Trial. Continuous glucose monitoring devices have become available in recent years and are now more widely covered by insurance.14 Some systems integrate with insulin pumps to allow for round-the-clock monitoring of blood glucose.15 A small glucose sensor is inserted subcutaneously, and it sends data to the insulin pump via a radio-frequency transmitter. Glucose is measured from the interstitial tissue every minute, and average values are displayed every five minutes. Meter testing is still required for calibrating the system and ensuring the values are accurate before taking corrective actions. The system has an alarm function to alert when there are variations in glucose levels outside of the customizable, pre-programmed desired range. These alarms prompt the patient to correct fluctuations such as hypoglycemia and hyperglycemia promptly, thus preventing potential complications. It is the hope that someday this technology can be integrated fully with the pump — in essence, creating an external pancreas.
Other pharmacological agents. The American Diabetes Association recommends other beneficial pharmacological agents for patients with type 1 diabetes2 used for treatment or prevention of cardiac and kidney complications. The medications and their purposes are outlined in Table 3. Clinicians should keep in mind side effects of certain medications, such as masking of hypoglycemia symptoms that occur with beta-blockers, decreased cardiac response with calcium channel blockers, and myalgia from statin medication.11
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Table 3: Common Diabetes Complications and Usual Pharmacologic Management2 | |
|
Diabetes Complication |
Pharmacologic Therapy and Purpose |
|
Cardiovascular disease • Hypertension (common comorbidity in diabetes and in type 1 diabetes, is usually the result of underlying nephropathy) |
• Either angiotensin converting enzyme (ACE) • Two or more agents at maximal doses |
|
• Dyslipidemia/lipid management |
Statin therapy • With overt cardiovascular disease • Without overt cardiovascular disease who are >40 years old and have one or more other cardiovascular disease risk factors • Statin therapy is contraindicated in pregnancy |
|
• Increased cardiovascular risk |
Antiplatelet therapy • Aspirin; primary prevention in type 1 diabetes at increased risk, including those over 40 years of age or those who have additional risk factors; secondary prevention in those with history of cardiovascular disease. Not recommended in people under 30 years of age. • Clopidogrel if allergic to aspirin • Combination therapy with the two agents for up to one year after an acute coronary syndrome B-blockers to reduce mortality in patients with prior myocardial infacrtion. |
|
• Nephropathy |
ACE inhibitors or ARBs • To delay the progression of nephropathy • To reduce cardiovascular disease pitcp,es (i.e., myocardial infarction, stroke, death) • Prevention of albuminaria Diuretics, calcium channel blockers, betablockers • As additional therapy to further decrease blood pressure. |
Diabetes self-management education. Perhaps the most important part of the medical management of type 1 diabetes is diabetes self-management education, which provides the patient with assistance from healthcare professionals whose expertise is in diabetes.13 The intended key outcome of this education is for patients to maintain effective self-care of their diabetes as life-changes that alter glycemic control emerge and new treatment advances become available.2 Certified diabetes educators teach patients how to adjust insulin to avoid the adverse effects of exercise, optimize glycemic control, recognize and treat hypoglycemia, prevent complications, and maximize quality of life. Many states mandate the cost of diabetes education be covered by insurance, as are medications and supplies.13
Special Considerations in Physical Therapy Management
Patients presenting to physical therapy after an injury or surgery will need more frequent glucose monitoring during the recovery process. Illness, trauma, and the physiologic stress of surgery can make glycemic control more difficult due to periods of physical inactivity and symptoms that accompany illness, such as nausea and vomiting, which can lead to hyperglycemia or hypoglycemia respectively.8 Significant elevations in blood glucose will require temporary adjustments in insulin requirements by the diabetes team. Patients with type 1 diabetes referred to physical therapy should be questioned regarding any changes in glycemic control since the injury or surgery. The effect of such physical or mental stress is likely to upset glycemic control and needs to be addressed within physical therapy treatment to promote optimal tissue healing, positively influence the rehabilitative process, and maximize rehabilitation outcomes.Although beneficial in improving glucose control and helping retard development of complications, patients with type 1 diabetes can find exercising challenging. The net effect of exercise on blood glucose levels is dependent on pre-exercise levels of glycemia, type and duration of exercise, and timing of medications and food intake.16 Based on the interaction of these factors, exercise may precipitate or worsen hypoglycemia or hyperglycemia. Knowledge of these interactions, along with frequent blood glucose monitoring, can reduce the likelihood of harmful blood glucose fluctuations during exercise.
Hypoglycemia, or low blood sugar, is the most common acute complication of diabetes. It is defined as a blood glucose level less than 70 mg/dl.8,17 The causes are related to insulin-food-activity mismatch. Not recognizing the symptoms of hypoglycemia, ignoring them, or not acting on them quickly enough can lead to severe hypoglycemia, which is the point at which the individual is unable to treat him or herself. A glucagon injection kit is needed for treatment of severe hypoglycemia. Glucagon for injection is a polypeptide hormone identical to human glucagon that raises blood glucose by converting liver glycogen into glucose.18 All patients should have a kit prescribed, and PTs should be familiar with its administration. Table 4 reviews instructions on preparing and administering glucagon.
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Table 4: Step-by-Step Instructions* on Glucagon Administration for Severe Hypoglycemia18,39,40 |
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1. Activate emergency medical system. 2. The glucagon kit contains either (a) a pre-filled syringe and a vial of glucagon powder or (b) a syringe, one vial with liquid, one vial with glucagon powder. Prepare according to directions included in package insert. · If a, inject the liquid from the syringe into the vial with glucagon powder. · If b, draw liquid from vial with the syringe and inject it into the glucagon powder vial. · Remove the syringe from the bottle. Gently shake the mixture in the vial until the glucagon powder is dissolved and the solution becomes clear and of a water-like consistency. 3. Draw the mixture back into the syringe. Follow instructions for dosing below. · For adults or pediatric patients weighing more than 44 lb (20 kg) withdraw all of the solution; 1 mg (1 unit) · For children weighing less than 44 lb (20 kg) give .5 mg (0.5 unit) 4. Inject glucagon into the arm, thigh or buttock. Turn the person on his or her side as glucagon may cause nausea and/or vomiting. The person should regain consciousness within 15 minutes. The person may eat when conscious and able to swallow. Notify healthcare professional. * An instructional video on preparing and administering glucagon is available at http://www.diabetes.org/type-1diabetes/hypoglycemia.jsp. |
Hypoglycemia unawareness can occur with long-standing diabetes because people lose their sensitivity to symptoms or feel them at much lower blood glucose levels;19 this mechanism has been found to be impaired in insulin-dependent people after two to five years with the disease. It is believed to be caused by neuropathic changes, which suppress the release of adrenaline, the hormone that triggers some of the symptoms. The neuroglycopenic (central nervous system) symptoms may be the only indicators of low blood sugar in people with hypoglycemia unawareness. Table 5 lists common symptoms, corresponding origin from the nervous system, and treatment of hypoglycemia. Recovery from hypoglycemia is dependent on symptom recognition and release of endogenous glucagon in response to dropping blood glucose levels, which signals the liver to release glucose into the bloodstream.
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Table 5: Recognizing and Treating Hypoglycemia and Hyperglycemia13,17,19,20,22,23 | ||
|
BG level |
Symptoms |
Treatment |
|
Mild hypoglycemia <70 mg/dl or below 90 with symptoms |
Sympathetic nervous system — · Sweating · Shaking · Excessive hunger · Paleness · Rapid or pounding heart beat · Nervous anxiety · Numbness/tingling around the lips or mouth Central nervous system — · Poor concentration · Mood changes · Irritability · Behavioral changes · Impaired judgment · Slurred speech · Staggering gait · Double or blurred vision |
15 grams of fast-acting carbohydrate and rest for 15 minutes · 3to 4 glucose/dextrose tablets (4g CHO each) · 4 oz (½ cup) no added sugar fruit juice · ½ can of regular soda · 6 to 8 gummy or regular Life Savers® · 1 Tbsp. sugar or jelly |
|
Severe hypoglycemia External help needed, blood glucose levels will vary. |
Loss of consciousness, inability to treat on his or her own, inability to coordinate or follow directions. |
Activate If no glucagon kit available, activate |
|
Hyperglycemia >160 mg/dl |
Polyurea (increased urination) Fatigue Polydipsea (extreme thirst) Polyphagia (excessive eating) High glucose in the urine Blurred vision |
If =250 mg/dl check for ketones. With moderate to large ketones, follow instructions from physician. May be caused by not enough insulin, too much food, and illness. Correction bolus (supplemental insulin) and continue self-monitoring of blood glucose every three to four hours. If not improved after three days and remains >180 will likely need insulin dose adjustment. |
|
Ketoacidosis Life-threatening if not corrected |
Shortness of breath, Fruity-smelling breath, Nausea and vomiting, A very dry mouth |
Need to contact physician if ketones are moderate to large. Can lead to dehydration and can lead to unconsciousness. |
The “15/15 Rule”20 is followed for treatment of conscious (mild) hypoglycemia. Fifteen grams of fast-acting carbohydrate is consumed, and blood glucose is reassessed in 15 minutes; glucose tablets or juice are recommended. If blood glucose is still below 70 mg/dl, treatment should be repeated with an additional 15 grams of carbohydrate. If the next meal to be consumed is more than an hour away, a snack consisting of an additional 15 grams of carbohydrate should be consumed to prevent blood glucose from falling again. The foods used to treat hypoglycemia should not include fat, such as a candy bar, as fat slows carbohydrate metabolism and will delay the rise in blood glucose. Glucose tablets should be available in physical therapy outpatient facilities, perhaps kept with the first-aid kit.
Low- to moderate-intensity exercise of at least 30 minutes duration21 lowers blood glucose in people with diabetes when pre-exercise levels are within normal ranges. The glucose lowering effects of exercise can be apparent in several hours and last up to 24 hours or more,20 after the activity due to prolonged enhancement of insulin sensitivity and altered counter-regulatory response from the liver. Furthermore, hypoglycemia is more likely to occur after a previous episode of low blood sugar. Although the propensity for hypoglycemia in insulin-dependent diabetes is influenced by many factors, such as type and duration of insulin and exercise, safeguards can be taken to minimize the possibility of hypoglycemic episodes.
Patients should monitor blood glucose levels shortly before, during, and immediately after exercise. To help assess the response and tolerance to exercise and determine necessary adjustments in management, they should also monitor blood glucose several hours after exercise. Strategies to prevent hypoglycemia with exercise include decreasing insulin dosing, carbohydrate supplementation, or using a lower temporary basal rate in the pump. Reducing insulin dosage to prevent hypoglycemia may cause a rebound effect during the recovery period after exercise, resulting in elevated blood glucose levels — yet this is more easily managed than acute hypoglycemia. If patients have not received education on how to make these adjustments, they should be referred to a diabetes specialist for discussion.
Hyperglycemia is defined as blood glucose above 160 mg/dl; it is also the result of insulin-food-activity mismatch.22 Hyperglycemia may arise after a hypoglycemic episode, from overtreating it (too much carbohydrate), or from counter-regulatory hormones such as glucagon, cortisone, and epinephrine.8 Morning hyperglycemia can also occur if there was night-time hypoglycemia or from the “dawn phenomenon,” which is caused by early morning elevations of growth hormone. Patients may find elevated blood glucose after strenuous (high-intensity) exercise from too much carbohydrate supplementation, or lower levels of insulin during recovery, because insulin modulates the rate of muscle glucose uptake.15 Type 1 diabetics may perform high-intensity exercise, but they should keep the potential for hyperglycemia in mind and monitor pre-activity blood glucose levels. Insulin supplementation may be needed after high-intensity exercise.15 Managing hyperglycemic episodes is also imperative in diabetes control and should be monitored during treatment sessions. Although not considered and immediately life-threatening complication of diabetes, hyperglycemia is what leads to vascular and tissue changes causing the well-known diabetes complications. When there is not enough exogenous insulin the body is unable to metabolize and use carbohydrate as an energy source which stimulates fat to be converted to energy to maintain body functions. Ketones are byproducts of fatty acid utilization for energy.23 Once formed, ketones appear in the bloodstream and also spill into the urine causing dehydration.
In patients with type 1 diabetes, exercise alone will not lower pre-exercise hyperglycemia; insulin supplementation will be necessary to correct hyperglycemia. Patients should not exercise aerobically with hyperglycemia and when ketones are present as this could precipitate further increases in blood glucose from increased energy demand in the tissues. This situation may also lead to diabetic ketoacidosis, which is considered a medical emergency. Ketone testing is recommended when blood glucose is above 250 mg/dl. Symptoms of hyperglycemia and management are summarized in Table 5.
Poor glycemic control may lead to loss of protective sensation, which can appear before diabetic neuropathy. The neurological exam recommended by the American Diabetes Association is designed to identify loss of protective sensation. It consists of monofilament testing and at least one other test, including pinprick sensation, vibration perception (using a 128-Hz tuning fork), and ankle reflexes. Pedal pulses should be palpated as well.2,24
Corticosteroid injections may be used in the management of certain musculoskeletal conditions, and physicians may not tell about the deleterious effect of these agents on glycemic control.25 Hyperglycemia will likely ensue after injection of soft tissues or peritendinous areas requiring the patient to perform more frequent self-monitoring of blood glucose and increase insulin requirements. The effects can begin within 24 hours and continue from five to 21 days.26,27,28
Some patients may not be as capable in self-management and will need assistance in problem-solving so they can safely and successfully complete therapy sessions, and some patients will require additional help from their diabetes specialist. Management of the type 1 diabetes patient in the physical therapy clinic needs to be individualized based on blood glucose measurements and the type of exercise to be performed. It will take some trial and error and a multidisciplinary approach to optimize treatment outcomes and maintain patient safety.
Lesser-known diabetes complications. Certain conditions and syndromes occur more frequently in people with diabetes compared to the general population. Clinicians may place little emphasis or give little consideration to how poor glycemic control may manifest itself in musculoskeletal disorders. These conditions would manifest themselves in patients with type 1 diabetes due to the cumulative effect of poorly controlled diabetes. Table 6 lists disorders, characteristics or physical findings, incidence, and management as presented in the literature.
The mechanisms by which musculoskeletal manifestations present in diabetes are not clearly understood, but glycosylation of proteins, microvascular abnormalities leading to damage to blood vessels and nerves, and collagen accumulation in the skin and periarticular structures are purported to cause changes in connective tissue.26,29,30,31,32 Commonly seen conditions in outpatient orthopedic physical therapy practices that emerge from these processes include diabetic cheiroarthopathy (diabetic stiff hand syndrome), flexor tenosynovitis (trigger finger), Dupytren’s contracture, adhesive capsulitis (frozen shoulder, diabetic stiff shoulder), calcific periarthitis, and complex regional pain syndrome.32,33,34 Musculoskeletal complications are said to be more common in type 1 diabetes but also occur in patients with type 2 diabetes.30 Furthermore, the literature notes people with diabetes are more recalcitrant to conservative treatment and have poorer outcomes with the conditions listed above.26,35,36
Diabetic osteoarthopathy (neuropathic arthropathy or Charcot’s disease) arises from underlying diabetic neuropathy.29,30,31,32,34 Osteoporosis and osteopenia are theorized to be more common in people with diabetes due to decreased insulin-like factor and impaired calcium absorption, leading to lower bone mineral density.31,32,37 Post-menopausal women with type 1 diabetes have an increased risk of hip fracture.34,37 and osteolysis of the foot is associated with osteoporosis.32 Diffuse idiopathic skeletal hyperostosis (ankylosing hyperostosis) also occurs more frequently in patients with diabetes due to metaplastic calcification of spinal ligaments and osteophyte formation , which limits range of motion in the neck and back.26,31,34 Diabetic muscle infarction and diabetic amyotrophy occur in type 1 diabetes and type 2 diabetes respectively; infarction presents as acute onset of pain and swelling over the affected muscle groups, and amyotrophy presents as acute muscle weakness and wasting.29,31,34 Patients on statin therapy may also present with myalgia, which is muscle tenderness or stiffness from rhabdomyolisis.31,38
The physical therapy profession has focused on type 2 diabetes, perhaps because it is preventable or modifiable and encompasses the majority of patients with diabetes. When type 1 diabetes is addressed specifically, complications such as diabetic neuropathy or ulcers dominate the literature. The physical therapy profession would benefit by establishing a standard of care for patients with type 1 diabetes that can improve patient safety and lead to more appropriate prognosis and outcomes. Diabetes management in physical therapy needs to be specific to the particular type, not all patients with diabetes lumped into one homogenous group. PTs should be comfortable with the self-monitoring of blood glucose and interpretation of values as related therapy interventions, and they should be prepared to treat hypoglycemia. Patients will benefit from the clinicians’ involvement by providing encouragement of performing self-care skills and exercising active problem solving. Referral to the diabetes specialist should be done when the patient is lacking these skills.
Comprehensive outpatient physical therapy care of a patient with type 1 diabetes requires special considerations and knowledge. Contemplation of key differences in etiology and management of type 1 diabetes from other types of diabetes, guidelines for self-monitoring of blood glucose and insulin therapy, hypoglycemia and hyperglycemia recognition and treatment, the musculoskeletal manifestations of diabetes mellitus, and the effects of exercise on blood glucose will guarantee individualized and thoughtful service delivery by clinicians.
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Musculoskeletal Complications of Diabetes28,29,30,31,32,33,34,37 | |||||
|
Disorder |
Other names |
Characteristics |
Cause |
Incidence |
Management |
|
Diabetic cheiro-arthropaty |
Diabetic stiff hand syndrome, diabetic hand syndrome |
Tight, waxy, thick skin. Limited range of motion in the fingers. Positive “prayer sign”. |
Increased glycosylation of collagen in the skin, nerve and vascular impairments, decreased collagen degradation. |
8% to 50% of patients with T1DM but may also be seen in patients with T2DM |
Optimize glycemic control. Range of |
|
Flexor tenosy-novitis |
Trigger finger |
Palpable nodule under the metacarpal head, thickening along affected flexor tendon sheath. Patient may report a catching sensation or pain |
11% to 16% |
Corticosteroid injections, physical therapy, NSAIDs. Surgery may be needed if conservative treatment fails in order to restore | |
|
Dupytren’s contracture |
|
Palmar fascia becomes thickened and shortened. Fibrosis and nodules are present in the fascia. Ring and middle finger most affected in patients with diabetes. |
16% to 63% Most common musculoskeletal complication of diabetes in the hand |
Mild cases benefit from PT. Local corticosteroid injections. Surgery for more severe cases. | |
|
Carpal tunnel syndrome |
|
Weakness and atrophy of thenar musculature in moderate to severe cases. |
Connective tissue changes from glycosylation of proteins and vascu lar changes lead to median nerve entrapment. Usually bilateral in diabetes. |
Up to 20% of patients with diabetes. |
Management is the same as for non-diabetics. Improve glycemic control. |
|
Adhesive capsulitis |
Frozen shoulder |
Stiffness and global ROM limitations. May be bilateral or involve the non-dominant side. |
Limited joint mobility due to glucose-induced collagen modifications, fibrosis. (Cagliero) |
11% to 30%. Appears at a younger age than the general population, may be less painful. |
Corticosteroid injection in the painful initial stage. NSAIDs. PT after the painful stage throughout the condition to restore function. Manipulation under anesthesia or surgical release of the capsule may be needed. More resistant to treatment in people with diabetes. |
|
Calcific Periarthritis |
Hydroxyapatite deposition disease (HADD), calcific tendonitis |
May be asymptomatic in two-thirds of cases due to sensory loss. May present as a painful shoulder with limited ROM. Radiograph with findings of calcium deposits around the rotator cuff area. |
Vascular diabetes complications, decreased blood flow, may precipitate tendon calcification. Inhibition of collagen synthesis from insulin deficiency may also lead to calcification of connective tissue. (Mavrikakis) |
Three times more likely in patients with diabetes than the general population. |
Physical therapy modalities and therapeutic exercise to decrease pain and restore |
|
Complex regional pain syndrome |
Reflex sympathetic dystrophy, diabetic shoulder-hand syndrome. |
Diffuse or localized upper extremity pain, edema, skin and vasomotor changes, and hyperesthesia. |
Increased expression of cytokines, fibroblast proliferation. |
Incidence in patients with diabetes has not been established. May be associated with adhesive capsulitis. |
Treatment recommendations are the same as for people without diabetes. |
|
Diabetic osteo-arthropathy |
Neuropathic arthopathy, Charcot’s disease |
Loss of sensation and proprioception in the lower extremities. Painless edema, deformity of tarsometatarsal joint, hyperpigmentation or purpura, erythema, joint laxity, soft tissue ulcers over the affected area. Normal motor function. |
Underlying diabetic neuropathy. |
Rare for both T1DM and T2DM, 0.1% to 2.5%. |
The lower extremity weight-bearing joints are more commonly affected and treatment consists of bracing, improving glycemic control and unloading the joint. Antibiotics may be prescribed if skin ulcerations are present. |
|
Osteolysis of the foot |
|
Cortical destruction of bone sparing the central diaphisis. |
Associated with osteoporosis |
|
Immobilization of the joints and limiting weight bearing as for diabetic osteoarthropathy. |
|
Diabetic muscle infarction |
|
Acute onset of pain and swelling ver affected muscle groups. |
Long-standing and poorly controlled T1DM. Considered a complication of advanced atherosclerosis. |
Rare. Patients are also likely to have coexisting neuropathy, nephropathy and retinopathy. |
Physical therapy may cause exacerbation. Treatment involves rest and pain relief measures. Recovery is spontaneous. |
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Diabetic amyotrophy |
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Muscle weakness and wasting, diffuse proximal lower extremity muscle pain, asymmetrical loss of tendon jerks. May involve the shoulder girdle. |
Cause is unknown. |
Older men with T2DM. Incidence is unknown. |
Physical therapy may be used to regain muscle function. Improving glycemic control and pain management are part of the treatment. Recovery may take up to a year. |
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Rhabdo-myolisis |
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Myalgia, muscle tenderness or stiffness, aching. |
Statin-related muscle pain. Skeletal muscle cells break down, releasing myoglobin, which is toxic to the kidneys. |
Any patient on statin therapy. |
Laboratory testing of creatinine kinase levels confirm diagnosis. Patients are |
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Osteoporosis and osteopenia |
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Decrease in insulin-like factors and impaired intestinal calcium absorption lead to lower bone mineral density. |
Post-menopausal women with T1DM have greater risk of hip fracture. |
Improve glycemic control. |
|
Diffuse idiopathic skeletal hyperostosis (DISH) |
Ankylosing hyperostosis |
Stiffness in the neck and back with limited ROM. Metaplastic calcification of spinal ligaments with osteophyte formation, mostly in the thoracic spine. |
Pathophysiology is unknown but thought to be related to high levels of insulin and insulin-growth factor which stimulates bone growth. |
Type 2 diabetes obese patients with metabolic syndrome and type 1 diabetes have been documented. 13% to 49% incidence with diabetes. |
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