PATHOLOGY: Implications for the Physical Therapist

Atherosclerosis.: Because of the hyperglycemia and increased fat metabolism associated with type 1 DM, atherosclerosis begins earlier and is more extensive among people with diabetes than in the general population. Atherosclerotic changes in large blood vessels, caused by lipid accumulation and thickening of vessel walls, result in decreased vessel lumen size, compromised blood flow, and ischemia to adjacent tissues. As a consequence, people with diabetes have a much higher risk of myocardial infarction, stroke, and limb amputation.

Atherosclerosis and the accompanying large-vessel changes result in cardiovascular and cerebrovascular changes, skin and nail changes, poor tissue perfusion, decreased or absent pedal pulses, and impaired wound healing. Atherosclerosis combined with peripheral neuropathy and the subsequent foot deformities increases the risk for ulceration of skin and underlying tissues and limb amputation.

Individuals with undiagnosed type 2 DM are at significantly higher risk for CAD, stroke, and peripheral vascular disease than the population without diabetes. Screening of the type 2 at-risk population is essential in the prevention and treatment of diabetes-related complications. In addition, all individuals with diabetes should be aware of the strong and consistent data regarding the risks of smoking and the exacerbation of atherosclerosis-related diabetic complications.

Clients and families should be consistently and continuously counseled and encouraged in smoking cessation. The combination of smoking and diabetes dramatically increases the risks related to atherosclerotic vessel disease, impaired wound healing, and the associated morbidity and mortality rates.⁵

Cardiovascular Complications.: CVD is the leading cause of mortality and morbidity in diabetes and accounts for approximately two-thirds of all deaths among the diabetic population.⁴¹ People with diabetes have 1.5-to 4-fold increased risk of having CAD, stroke, and myocardial infarction.⁴¹ Although diabetes has long been recognized as a potent and prevalent risk factor of ischemic heart disease caused by coronary atherosclerosis, only recently has diabetes become associated with left ventricular dysfunction independent of hypertension and CAD. This is a disease of a cardiac muscle itself and is called diabetic cardiomyopathy.⁷¹

Left ventricular diastolic and systolic dysfunction, left ventricular hypertrophy, and alterations in the coronary microcirculation have all been observed in diabetic cardiomyopathy and are not fully explained by the cellular effects of hyperglycemia alone. The most important mechanisms of diabetic cardiomyopathy are metabolic disturbances, myocardial fibrosis, small vessel disease, cardiac autonomic neuropathy, and insulin resistance.⁷¹ Because of the presence of autonomic neuropathy, people with diabetes may have what is called “silent ischemia” or silent heart attack. They do not experience typical pain because of the damage to nerves that occurs in diabetes.

The cardiovascular and renal systems are intricately connected and affected by diabetes. Low blood flow to the kidney causes a release of renin, which in turn triggers a cascade of events as angiotensin is converted to angiotensin I then to angiotensin II, resulting in large increases in blood pressure. The risk of myocardial infarction and stroke increases as well.

Retinopathy and Nephropathy.: Diabetic retinopathy is a highly specific vascular complication in persons with both type 1 and type 2 DM and its prevalence is correlated closely with duration and control of high blood glucose levels. After 20 years with DM, nearly all individuals with type 1 DM and more than 60% of type 2 DM have some degree of retinopathy.

Diabetic retinopathy poses a serious threat to vision. Underlying microvascular occlusion of the retina resulting in progressive areas of retinal ischemia and tissue death causes diabetic retinopathy. Studies have established that intensive management of blood glucose level control to consistent near-normal levels can prevent and delay the progression of diabetic retinopathy.⁵⁵

Diabetes is now the leading cause of end-stage renal disease (ESRD), which is kidney failure requiring dialysis or transplantation, in the United States and Europe.¹⁷¹ Hardening and thickening of the glomerular basement membrane, which result in eventual destruction of critical renal filtration structures, cause diabetic nephropathy. The presence of small amounts of albumin in the urine is the earliest clinical evidence of nephropathy. The eventual destruction of the filtering ability of the kidney causes chronic renal failure and the need for permanent dialysis or renal transplantation.

Renal destruction, as with retinopathy, can be slowed significantly with early detection and monitoring, tight glucose control, early treatment of hypertension (particularly with angiotensin-converting enzyme [ACE] inhibitors), careful monitoring of dietary protein, and strong encouragement of cessation of smoking.^55,60,102 Hypertension is managed with ACE inhibitors initially and if blood pressure is not less than 130/85 mm Hg, a β-blocker may be added. However, combining a β-blocker with a diuretic can blunt awareness and symptoms of low glucose, so this combination usually is not recommended.

Infection.: Chronic, poorly controlled diabetes mellitus can lead to a variety of blood vessel and tissue changes that result in impaired wound healing and markedly increased risk for infections. Impaired vision and peripheral neuropathy contribute to the decreased ability of the person with diabetes to feel or see breaks in skin integrity and developing wounds. Vascular disease contributes to tissue hypoxia, which further decreases healing ability.

In addition, once pathogens are inside the body, they multiply rapidly because the increased glucose content in body fluids and tissues fosters bacterial growth. Because the blood supply to tissues is already compromised, white blood cells are not mobilized to the affected areas efficiently or adequately. Diabetes results in higher incidences of skin, urinary tract, vaginal, and other types of tissue infections.¹¹¹

Musculoskeletal Problems.: Musculoskeletal complications are common, often involving the hands, shoulders, spine, and feet. Carpal tunnel syndrome, Dupuytren’s contracture, trigger finger, and adhesive capsulitis occur four times more often in people with diabetes compared with those who do not have diabetes.^30,32 Available data show that more than 30% of people with type 1 or type 2 DM have some kind of hand or shoulder disease. More people with type 1 DM have musculoskeletal disorders than those with type 2 DM and the degree of stiffness is greater with this type of diabetes. The exact mechanism by which the specific metabolic abnormalities of diabetes are linked to rheumatic manifestations remains unclear.³¹

Although these disorders are not life-threatening, they can add significant functional impairment to a person’s life. See also the discussion of orthopedic problems that can develop secondary to sensory and motor neuropathy in the section on Sensory, Motor, and Autonomic Neuropathy in this chapter.

UPPER EXTREMITY.: In the hand, the syndrome of limited joint mobility (SLJM or LJM) and the stiff hand syndrome are unique to diabetes. SLJM is characterized by painless stiffness and limitation of the finger joints (Fig. 11-10). Flexion contractures typically progress to result in loss of dexterity and grip strength. The SLJM is an underdiagnosed complication of diabetes, largely because this type of loss of hand range of motion is considered a common normal sign of aging.⁸⁹ The severity of this syndrome in diabetes is correlated with the duration of disease, duration and quantity of insulin therapy, and smoking. Joint contractures also may develop in larger joints, such as the elbows, shoulders, knees, and spine.

Figure 11-10 The prayer sign. The individual is unable to press the palms flat against each other, a diagnostic sign for the syndrome of limited joint mobility in diabetic persons. Other conditions also may result in loss of extension with a positive prayer sign. (From Kaye T: Watching for and managing musculoskeletal problems in diabetes, J Musculoskel Med 11:25-37, 1994.)

The stiff hand syndrome often is confused with or included in SLJM, but it has a distinct pathogenesis and clinical presentation. The stiff hand syndrome occurs uniquely with diabetes and is seen more frequently with type 1 DM and poor blood glucose control. Paresthesias, which eventually become painful, are accompanied by subcutaneous tissue changes such as stiffness and hardness. Vascular insufficiency may be the underlying cause or may be secondary to neuropathy, nodular tenosynovitis, and osteoarthritis.

Dupuytren’s contracture is characterized by the formation of a flexion contracture, palmar nodules, and thickening band or cord of palmar fascia (Fig. 11-11), usually involving the third and fourth digits in the population with diabetes (rather than the fourth and fifth digits in the population without diabetes). Pain and decreased range of motion are the primary presentation. Painless nodules develop in the distal palmar crease, often in line with the ring finger, which slowly mature into a longitudinal cord that is readily distinguishable from a tendon. The skin overlying the nodules is usually puckered.

Figure 11-11 Dupuytren’s contracture. Painless nodules develop in the distal palmar crease, often in line with the ring finger, that slowly mature into a longitudinal cord that is readily distinguishable from a tendon. The skin overlying the nodules is usually puckered. The contracture may be symptomatic (painful), but with or without pain it results in impaired hand function. (From Kaye T: Watching for and managing musculoskeletal problems in diabetes, J Musculoskel Med 11:25-37, 1994.)

In some cases, regression of symptoms does occur without intervention, although the underlying mechanism for this phenomenon remains unknown. Surgical excision has not been shown to be a reliable cure for the disease and is not recommended unless there is a contracture that is bothersome. It has been reported that if the disease recurs after surgical excision, the rate of progression may be faster.²⁰⁴

Flexor tenosynovitis (also called chronic stenosing tenosynovitis) is another rheumatologic condition seen more commonly in persons with diabetes. Tenosynovitis is caused by accumulation of fibrous tissue in the tendon sheath and can cause aching, nodularity along the flexor tendons, and contracture. Locking of the digit, called trigger finger, can occur in flexion or extension and may be associated with crepitus or pain. In the population with diabetes, tenosynovitis is found predominantly in women and affects the thumb, middle, and ring fingers most often.

Diabetes is the systemic disease most often seen in connection with peripheral neuropathy of the hand, including CTS. The clinical presentation of CTS is the same for the person with diabetes as for the person without diabetes, although in diabetes CTS can be either a neuropathic process or an entrapment problem. Both neuropathy and compression within the carpal tunnel may exist together.

Adhesive capsulitis (also known as periarthritis or frozen shoulder) is characterized by diffuse shoulder pain and loss of motion in all directions, often with a positive painful arc test and limited joint accessory motions. The pattern is slightly different from that of typical adhesive capsulitis, in which regional tightness in the anteroinferior joint capsule primarily compromises external rotation, followed by loss of abduction and less often, internal rotation and flexion.

The pattern in diabetes is one of significant global tightness with external and internal rotation equally limited in the dominant shoulder, followed by limitations in abduction and hyperextension. External rotation and hyperextension are most limited in the nondominant shoulder, followed by internal rotation and abduction. The pathogenesis of the capsular thickening and adherence to the humeral head remains unknown. The long head of the biceps tendon may become glued down in its tendon sheath on the anterior humeral head.²³⁹

Adhesive capsulitis may be accompanied by vasomotor instability of the hand previously referred to as reflex sympathetic dystrophy (RSD) but now classified as the complex regional pain syndrome (CRPS). This condition is characterized by severe pain, swelling, and trophic skin changes of the hand (e.g., thinning and shininess of the skin with loss of wrinkling, sometimes with increased hair growth).

Skin changes in diabetic hand arthropathy, in addition to changes caused by CRPS, may occur in association with adhesive capsulitis. Other skin changes associated with diabetes include scleroderma diabeticorum, an asymptomatic thickening of the skin that may lead to a peau d’orange appearance, which usually involves the posterior neck, upper back, and shoulders.²⁷

Skin and subcutaneous tissue atrophy and tendon flexion contractures develop. The natural history of this condition ranges from spontaneous remission to perma- nent loss of function. (See the section on Complex Regional Pain Syndrome in Chapter 39.)

Tendinopathy with thickening of the plantar fascia and Achilles tendon and tendo-Achilles tightening occurs as glucose deposits in tendons and ligaments result in loss of flexibility and rigid foot. In the diabetic population, loss of Achilles tendon flexibility, especially when combined with a flatfoot, increases pressure under the foot, adding to the compressive forces that contribute to ulcer formation.⁸²

SPINE.: Diffuse idiopathic skeletal hyperostosis (DISH; also known as ankylosing hyperostosis or Forestier disease) is a condition of the spine seen most often in people with type 2 DM, although it can occur in a person who does not have diabetes. In DISH, osteophytes develop into bony spurs, typically right-sided syndesmophytes that may join to form bridges (Fig. 11-12). The thoracic spine most commonly is involved. In contrast to ankylosing spondylitis, the sacroiliac joints are spared, and vertebral body osteoporosis is absent. Calcaneal and olecranon spurs may develop, and new bone may form around hips, knees, and wrists.

Figure 11-12 Diffuse idiopathic skeletal hyperostosis (DISH), or ankylosing hyperostosis, associated with type 2 diabetes mellitus (DM). DISH can occur with other conditions such as ankylosing spondylitis. Although the dense anterior bony bridging of the cervical vertebrae is pictured on this lateral roentgenogram, the thoracic spine most commonly is involved in diabetes. This type of DISH can be distinguished from ankylosing spondylitis by the preservation of sacroiliac joints, a site of typical involvement in ankylosing spondylitis. (From Kaye T: Watching for and managing musculoskeletal problems in diabetes, J Musculoskel Med 11:25-37, 1994.)

People with DISH may be asymptomatic or they may experience back pain and stiffness without limitations in range of motion. Dysphagia may develop if extensive cervical spine involvement occurs. The pathogenesis of DISH is unknown, and apparently no correlation exists between the degree of diabetic control and the extent of hyperostosis.

OSTEOPOROSIS.: Generalized osteoporosis usually develops within the first 5 years after the onset of DM and is more severe in persons with type 1 DM. It is hypothesized that bone matrix formation may be inadequate in the absence of normal circulating insulin levels. Results of bone density studies in persons with type 2 DM are conflicting, with some studies demonstrating decreased bone density and others indicating increased bone density. People with type 2 DM have decreased circulating insulin levels because of beta-cell exhaustion, and others are hyperinsulinemic because of insulin resistance.

As in any case of osteoporosis, regardless of the underlying cause, this condition places the person at greater risk for fractures. With the additional loss of sensation associated with diabetes, minor trauma easily produces injury. Microfractures can occur in already weakened bone and cartilage and may remain unrecognized because of the lack of pain appreciation. A vicious circle is started, leading to further damage.

Sensory, Motor, and Autonomic Neuropathy.: Sensory, motor, and autonomic neuropathy associated with DM is a common phenomenon with known risk factors (e.g., duration of diabetes, current glycated hemoglobin value [HbA1c, also written as Hb_A1c], BMI, smoking, hypertension, and high triglycerides). The presence of CVD doubles the risk of neuropathy.²⁴²

Neuropathy may affect the CNS, peripheral nervous system, or autonomic nervous system (see Box 39-5). The most common form of diabetic neuropathy is a sensory polyneuropathy, usually affecting the hands and feet and causing symptoms that range from mild tingling, burning, numbness, or pain to a complete loss of sensation (usually feet) and foot drop. See further discussion of diabetic neuropathy in Chapter 39.

SENSORY NEUROPATHY.: Many people with diabetes suffer from diabetic peripheral neuropathic pain (DPNP) associated with nerve damage. Spontaneous pain, allodynia (painful response to benign stimuli), hyperalgesia, and other unpleasant symptoms are common with DPNP. Neuropathic pain often progressively increases in intensity throughout the day and is worse at night, significantly impairing sleep. Some individuals experience painful neuropathy called insulin neuritis syndrome at the beginning of therapy for diabetes; the feet are affected more often than the hands and it is usually self-limiting.²⁵⁶

The loss of sensation in diabetic neuropathy predisposes joints to repeated trauma and progressive joint destruction. Chronic progressive degeneration of the stress-bearing portion of a joint associated with loss of proprioceptive sensation in the joint produces a condition called Charcot’s disease, Charcot’s arthropathy, neuroarthropathy, or neuropathic arthropathy. Diabetes is the most common cause of neuropathic joints.

Several stages of neuropathic arthropathy (Charcot’s foot) occur involving bone destruction and absorption leading to dislocation and an unstable joint. Bone fragments and debris are deposited in the affected joint. Subluxation of the tarsal and metatarsal joints commonly results in a rocker-bottom foot deformity (see Fig. 23-9) and a redistribution of pressure on the plantar surface of the foot with progressive ulceration. An acute neuropathic joint is swollen, warm, and edematous, but pain may be minimal because of the underlying altered sensation.

Left untreated, neuropathic changes can progress to complete destruction of the joint. The presence of autonomic neuropathy may hasten this process as the blood vessels are unable to respond appropriately (e.g., vasoconstrict) to even minor trauma. Prolonged and unregulated hyperemia in the foot may lead to excessive bone resorption resulting in decreased bone mineral density, further increasing the risk of bone and joint destruction.¹⁰⁰

Joints with less movement transmit abnormal forces through the foot to injure already damaged joints. This is especially true during walking, when large forces are placed on the midtarsal and tarsometatarsal joints. Obesity further increases these forces, and in the presence of any preexisting gait abnormalities or deformities, both create additional stress that compounds the condition.

Assessment of the underlying problem is important in planning the appropriate treatment intervention. For example, improving circulation may be a goal with macrovascular or peripheral vascular disease, whereas foot care and orthoses are more appropriate treatments for microvascular-caused neuropathy. The underlying neurologic disorder should be treated but this has no effect on the existing arthropathy. Reduction of weight bearing, joint immobilization, and joint protection are important conservative treatment tools. Surgical fusion can be performed if all else fails, but joint replacement is contraindicated in this condition.^36,212

MOTOR NEUROPATHY.: Motor neuropathy is more common with long-standing disease and produces weakness and atrophy; bilateral but asymmetric proximal muscle weakness is called diabetic amyotrophy. Diabetic amyotrophy leads to bony deformities (e.g., claw toes, severe flatfoot with valgus of the midfoot, or collapse of the longitudinal arch) that contribute to biomechanical changes in foot function resulting in abnormal patterns of loading. Pain and erythema of the forefoot may constitute forefoot osteolysis, which is sometimes considered another form of neuropathy distinguished from cellulitis or osteomyelitis by laboratory values (leukocyte count) and roentgenographic appearance.

AUTONOMIC NEUROPATHY.: Autonomic neuropathy is sometimes referred to as diabetic autonomic neuropathy (DAN) and affects nerves that innervate heart, lung, stomach, intestines, bladder, and reproductive organs. It may manifest itself through the loss of control of blood pressure, blood glucose levels, temperature, regulation of sweating (skin becomes dry and cracked with buildup of callus), and blood flow in the limbs. Skin changes such as these can create more openings for bacteria to enter. The combination of all three types of neuropathy can ultimately lead to gangrene and possible amputation, largely preventable with proper care (see Special Implications for the Therapist: Diabetes and Foot Care in this section).

Cardiovascular autonomic neuropathy (CAN) is manifested by the lack of heart rate variability in response to deep breathing and exercise, exercise intolerance, persistent sinus tachycardia, bradycardia, and postural hypotension. Stress testing should be considered before starting an exercise program, especially in the older adult.⁸ CAN may also result in reduced perception of ischemic pain, making a person with diabetes unaware of having a heart attack. This may delay appropriate medical treatment and lead to death.²⁵⁵

DAN may lead to hypoglycemia without awareness because of loss of the warning signs of hypoglycemia such as sweating and palpitations. Being unaware of hypoglycemia and unresponsive to it are troublesome metabolic complications because they impair the person’s ability to manage the disease and may result in death. Other forms of autonomic neuropathy include gastroparesis (decreased gastrointestinal motility accompanied by diarrhea and fecal incontinence), constipation, urinary tract infections (nerve damage can prevent the bladder from emptying completely, allowing bacteria to grow in the bladder and kidneys), urinary incontinence, and sexual (erectile) dysfunction.

ULCERATION.: Sensory neuropathy, occurring as a result of improper glucose metabolism and diminished vascular perfusion to nerve tissues, places the diabetic person at risk for the development of ulcers. Diabetic foot ulcers are caused primarily by repetitive stress on the insensitive skin with increased pressure and/or horizontal (shear) stress. Body weight and activity level increase the force that the foot must transmit, and this also may increase pressure and shear force, especially in the presence of an underlying bony prominence or foot imbalance. In addition, previously healed ulcers leave scars that transmit force to underlying tissues in a more concentrated manner and hold the fat pad locally so that it cannot function physiologically. As a result, it cannot transmit shear forces, and it becomes damaged easily.

The loss of autonomic nerve function eliminates the production of sweat, leaving the skin dry and inelastic. Changes in pressure and gait, fat atrophy, and muscle weakness are mechanical factors that, along with sensory neuropathy, influence the development of plantar skin abnormalities, especially ulceration.^21,229 Diabetes-induced changes in the skin are likely to contribute to ulceration because the collagen and keratin (a protein that is the principal constituent of epidermis, hair, and nails) may be glycosylated (saturated with glucose) with increased cross-linking, which makes the skin stiff. Keratin builds up in response to the increased pressure, covering the openings of unhealed ulcers, and cannot be removed as readily as normal keratin.

The areas most commonly affected by foot ulcers are the plantar areas of the metatarsal heads, the toes, and the plantar area of the hallux (Fig. 11-13). In the Charcot foot, the incidence of ulceration beneath the talus and navicular bones becomes more common because of the rigid rocker-bottom deformity.

Figure 11-13 Neurotrophic ulcers associated with diabetic neuropathy. (From Callen JP, Jorizzo JL: Dermatological signs of internal disease, Philadelphia, 1995, WB Saunders.)

MEDICAL MANAGEMENT

PREVENTION.

Prevention of obesity-related health problems, including type 2 diabetes, is a key focus of the medical community. Therapists play an important role in providing education on the beneficial effects of exercise combined with proper nutrition. Studies have clearly shown that people who incorporate physical activity and exercise into their daily lives are less likely to develop type 2 diabetes no matter what their initial weight. Adopting an activity program of 150 minutes weekly of moderate intensity activity (e.g., brisk walking) similar to what the Surgeon General advises is a key prevention strategy.^133-135

Studies using liposuction in the overall treatment of obesity point to the possibility of this treatment option to disrupt the pathway that brings about insulin insensitivity in the obese individual and thus prevent diabetes from developing. Fat removal by liposuction has been linked with modification of cardiovascular risk and vascular inflammatory markers in the obese individual with beneficial effects on insulin resistance as well.^67,188

SCREENING.

In response to the statistic that one-fourth of all new cases of DM under age 20 are diagnosed as type 2 DM, the Centers for Disease Control and Prevention (CDC) now recommends diabetes testing begin at age 25 years. The American Diabetes Association recommends universal screening at age 45 (earlier for high-risk groups such as non-Caucasians, obese individuals, and those with a family history of type 2 DM in a first-degree relative).

DIAGNOSIS.

Diagnostic assessment may include a variety of testing procedures, such as plasma glucose, glucose tolerance test, (see Table 11-13), and urine ketone levels, to name just a few (see Table 40-4). A diagnosis of diabetes is confirmed by symptoms of hyperglycemia and blood and urine glucose and ketone abnormalities. Current defined criteria for definitive diagnosis of diabetes mellitus are the following⁴¹:

Classic symptoms of diabetes (polyuria, polydipsia, and unexplained weight loss) plus a casual plasma glucose concentration of ≥200 mg/dl. (Casual is defined as any time of day without regard to time since last meal.)

Fasting plasma glucose (FPG) ≥100 mg/dl after no caloric intake for at least 8 hours. (If the FPG is repeated and continues to be 100 mg/dl on a subsequent day, a GTT does not need to be done to confirm diagnosis.)

2-hour postload glucose ≥200 mg/dl during an OGTT.

GLUCOSE MONITORING.

Glucose monitoring is not as crucial for a person who has an established pattern of activities and/or exercise. When a new activity is introduced, such as occurs in an exercise or rehabilitation program, monitoring blood glucose levels is recommended until the individual’s response to the change is known and predictable in maintaining stable blood glucose levels. New insulins and easier blood glucose monitoring have improved the ability to obtain much tighter control of blood glucose levels with fewer fluctuations and reduced risk of hypoglycemia. There are several methods used to monitor glucose immediately and over time.

Frequent self-monitoring by performing a direct blood sampling (fingerstick or laser technique) provides immediate monitoring of blood glucose levels and is an important management tool in the long-term treatment of this disease. Early screening and assessment of people at risk for diabetes are critical so that prevention and treatment of complications can be initiated before the onset of significant blood vessel and tissue damage.

The development of noninvasive testing methods to monitor glucose levels without the use of fingersticks is underway. One device already commercially available (the GlucoWatch G2 Biographer [GW2B]) is worn like a watch and uses electrical currents to obtain interval measurements of glucose levels in the skin. This type of reverse iontophoresis monitoring device prevents the invasive and often painful skin punctures by needle or laser, now in use for blood glucose monitoring.^56,175,223 Use of the GW2B has not been shown to improve glycemic control or reduce the frequency of severe hypoglycemia. Skin reactions and other problems may lead to decreasing use over time.³⁸ At least one study advised against relying on the GW2B during moderate to intense exercise.¹⁷⁹

A handheld, infrared meter with voice activation that gives verbal directions and a verbal read out for the visually impaired is also under investigation. Other technology in use or being actively researched includes nocturnal alarms using a real-time glucose sensor to alert parents and children of hypoglycemic and hyperglycemic events while sleeping or for adolescents and adults, glucose-sensing skin patches, tattoos, or contact lenses. The contact lens would allow the individual with diabetes to see changes in the color of the contact lens to give an indication of blood glucose levels.¹³

Glycated (glycosylated) HbA1c level is used to monitor blood glucose control over time (Table 11-14). A1C is not used to diagnose diabetes. It is taken every 3 months and provides an average of the person’s overall glucose control. The American Diabetes Association recommends a target A1c level as 7% or less. According to the U.K. Prospective Diabetes Study, a 1% reduction of the A1c level reduces the risk of heart attack by 14% or more. People with HbA1c concentrations less than 5% had the lowest rates of CVD and mortality.¹²¹

Table 11-14

Correlating A1C to Mean Plasma Glucose Levels.

Normal reference range for A1C is 4%-6%. The goal for clients with diabetes is below 7% (target level is 6.5); higher levels are linked with greater risk of diabetes-related complications. A1C level of 7 correlates to an average daily plasma glucose level below 170 mg/dl. It is not used to diagnose diabetes and should not be measured too often in those who are using it to measure glucose control. Two measurements a year are sufficient in anyone who is meeting goals of treatment and who has stable control, and a maximum of 4-6 measurements a year is sufficient in people whose treatment has changed, or who are not meeting treatment goals.²⁰⁵ Data from American Diabetes Association, 2006.

Another monitoring tool used by individuals with diabetes includes fructosamine testing. Although the A1C is more popular and more widely accepted, the American Diabetes Association recognizes the fructosamine test as helpful in situations where A1C cannot be measured reliably. Situations in which fructosamine may be a better monitoring choice than A1c include the following^4a:

• Rapid changes in diabetes treatment—fructosamine allows the effectiveness of diet or medication adjustments to be evaluated after a couple of weeks rather than months.

• Diabetic pregnancy—good control is essential during pregnancy and the needs of the mother frequently change during gestation; fructosamine measurements may be ordered with glucose levels to help monitor and accommodate shifting glucose and insulin requirements.

• Red blood cell (RBC) loss or abnormalities—an A1C test will not be accurate when an individual has a condition, such as hemolytic anemia or blood loss, that affects the average age of RBCs present. The presence of some hemoglobin variants may affect certain methods for measuring HbA1c. In these cases, fructosamine can be used to monitor glucose control.

• Individuals on dialysis when an average glucose level over the past 2 to 3 weeks is needed.

The fructosamine test is not useful as a screen for diabetes, since the fructosamine concentrations of well-controlled diabetics may overlap with those of individuals who do not have diabetes.

A standard reference range is not available for the fructosamine test. Because reference values are dependent on many factors, including age, gender, sample population, and test method, numeric test results have different meanings in different laboratories. The laboratory report will include the specific reference range for the test and the client’s results in comparison.

An elevated fructosamine level is an indication of higher than average blood glucose level. Like the A1C, the value of this test is in looking at trends over time but over a shorter period of time compared to A1C. Fructosamine results are very useful when monitoring change in glucose levels associated with alterations in diet or medications.

TREATMENT.

There is no widely available cure for diabetes. The goal of overall care for persons with diabetes is control or regulation of blood glucose. Many large-scale studies have shown that tight glucose control reduces the risk of vascular complications in both type 1 and type 2 diabetes. Early identification and intervention are strongly linked with risk reduction of late complications.¹⁴¹ Three key standards and goals in the treatment and self-management of DM include the following:

• HbA1c less than 7%

• Blood pressure less than 130/80 mm Hg

• Total cholesterol less than 200 mg/dl (low density lipoprotein [LDL] less than 100 mg/dl)

Data from the National Center of Health Statistics show that only 7.3% of adults with diabetes have achieved all 3 targets.²¹³ To help people with diabetes reach these goals, the National Diabetes Education Program has started an education program called Control the ABCs, in which A is HbA1c, B is blood pressure, and C is cholesterol). Education materials are available in English and Spanish and for Asian Americans and Pacific Islanders.¹⁷⁶ Therapists can help reinforce these concepts as part of their client education programs.

Data suggest that atherogenic and inflammatory mediators contributing to microvascular and macrovascular complications are elevated even before the onset of diabetes. There may even be a “metabolic memory” associated with these early changes. Comprehensive metabolic control instituted early may alter the natural history of diabetic complications by affecting this metabolic memory.¹⁴¹

Researchers continue to investigate drugs that would prevent the formation of fat cells, thereby reducing the problem of obesity before type 2 DM can develop. Studies of the use of gene therapy as a treatment for both types of diabetes are ongoing, utilizing a variety of approaches, such as direct delivery of the insulin gene to non–beta-cells, improving insulin secretion from existing beta-cells, and implanting genetically modified cells.^83,84,116 Experimental research is underway in the development of a vaccine for type 1 DM that may help stop the immune system attack of the insulin-producing beta-cells of the pancreas.²⁵⁸

Type 1 Diabetes Mellitus.: Type 1 DM requires exogenous insulin administration and dietary management to achieve tight (near normal) blood glucose control. With no circulating endogenous insulin, the effect of aerobic exercise in providing increased glycemic control for the person with type 1 DM may be limited. To date, studies of the effect of aerobic exercise in type 1 DM have shown mixed results. Regardless, exercise should be taken into account as part of the total picture in order to minimize the complications associated with diabetes.

The insulin dosage schedule varies depending on the individual’s age, level of compliance, and severity of diabetes (Table 11-15). Control over blood glucose levels dictates how “brittle” the diabetes is. Brittle diabetes (also known as labile or unstable diabetes) is a term used when a person’s blood glucose level often swings quickly from high to low and from low to high. The individual with wide glucose excursions is considered very brittle.

Table 11-15

Insulin Dosage Schedule

Poorly controlled diabetes is ideally treated with more frequent administration of insulin (e.g., four times per day), whereas other individuals may receive insulin once or twice daily, sometimes mixing different types of insulin (e.g., rapid-acting [human analog; Humalog]; short-acting [regular] with intermediate-acting [NPH] insulin). Humalog (Lispro) is a type of insulin that has rapid action. It works faster than short-acting insulin and must be taken with a meal to prevent hypoglycemia.¹¹⁵ From a therapist’s point of view, the client receiving more frequent dosages is less likely to develop hypoglycemia, especially when beginning an exercise program.

Insulin Pump.: An insulin pump also known as continuous subcutaneous insulin infusion (CSII) is now available to deliver fixed amounts of regular insulin continuously, thereby more closely imitating the release of the hormone by the islet cells. This lightweight, pager-sized device is worn conveniently in a pocket or on a belt clip (Fig. 11-14); a waterproof design makes swimming possible.

Figure 11-14 The programmable insulin pump. Compact and worn like a pager, the programmable insulin pump delivers fixed amounts of insulin continuously, based on blood glucose levels determined by regular fingerstick glucose monitoring. The device includes the pump itself (including controls, processing module, and batteries), a disposable reservoir for insulin (inside the pump), and a disposable infusion set, including a cannula for subcutaneous insertion (under the skin) and a tubing system to interface the insulin reservoir to the cannula. (Courtesy Mini-Med, Sylmar, CA, 2000.)

The insulin pump offers many advantages such as flexible eating and exercising schedules, fewer episodes of severe hypoglycemia (especially at night and for teenagers who sleep longer hours), and convenience of taking insulin without the social consequences of public injections, to name a few.⁴³ Although this type of insulin administration provides better control, it has some disadvantages. It cannot detect and respond to changes in the blood glucose level so the individual must continue to monitor glucose levels and make dosage adjustments. There is no long-term backup supply of insulin such as is available with long-acting insulin injections. If the pump malfunctions and the person is unaware of it, blood glucose levels can rise quickly, potentially leading to ketoacidosis. The pump wearer must still monitor blood glucose levels at regular intervals.

It cannot be removed for more than 1 hour, reactions to the needle are common, bleeding can occur at the sensor insertion site, and like any other mechanical device, it is subject to malfunction. Insulin pump technology is improving every year; new “smart” features are added to the designs to simplify the tasks involved in delivering an insulin bolus. Implantable pump options that can dispense insulin in constant, steady pulses throughout the day are being tested. This type of pump would eliminate the need for an open needle site in the skin. Penlike injection cartridges also are in use.¹²⁶

Inhaled Insulin.: In 2006, the Food and Drug Administration (FDA) approved the first inhaled insulin combination product, Exubera, an inhaled powder form of recombinant human insulin (rDNA), for the treatment of adults with type 1 and type 2 diabetes. The inhaled form of insulin offers some people with diabetes an alternative to the many daily injections. It is a short-acting insulin and does not eliminate insulin injections for type 1 diabetes, but it can reduce the daily number required.

The onset of action for inhaled insulin is 10 to 20 minutes, which is more rapid than that of either regular or lispro subcutaneous insulin, so the individual is instructed to take it no more than 10 minutes before meals to prevent hypoglycemia. Inhaled insulin reaches peak effectiveness within 2 hours and remains effective for up to 6 hours.²⁶⁸

Its use is contraindicated in cigarette smokers or anyone who has smoked in the past 6 months, since it is inhaled directly into the lungs rather than into the blood stream. Smokers absorb much more insulin this way than nonsmokers do, leaving them at risk of dangerously low glucose levels.²⁴¹

Inhaled insulin is not recommended for people with pulmonary disorders such as asthma, bronchitis, or emphysema. Potential disadvantages include erratic absorption, poor postprandial glucose control, and side effects such as cough, dyspnea, sinusitis, and pharyngitis.¹³⁹ Long-term effects remain unknown but are under investigation.

Research continues to find other forms of a pain-free insulin delivery system. Insulin pills, an insulin patch, and an oral (mouth) spray are under investigation.

Type 2 Diabetes Mellitus.: Type 2 DM is most often treated with diet and exercise, sometimes in conjunction with oral hypoglycemic drugs (OHDs); insulin occasionally is required. Exercise is a recognized therapy for the prevention of complications in type 2 DM. Numerous studies have shown a consistent positive effect of regular exercise training on carbohydrate metabolism and insulin sensitivity. Some of the beneficial effects include decreased need for insulin, prevention of CVD and obesity, management of hypertension, and reduction in very LDL (VLDL) cholesterol.^41,161

A plant-based diet is becoming more widely known for its potential effects and benefits in the prevention and treatment of type 2 DM. The use of whole-grain or traditionally processed cereals and legumes has been associated with improved glycemic control in individuals with diabetes and in individuals who are insulin-resistant. Long-term studies have shown that whole-grain consumption reduces the risk of both type 2 diabetes and CVD.¹¹⁴

The combination of diet and exercise is more powerful than either one alone and may be even more effective than drugs for preventing type 2 DM. A low-fat, low-calorie diet with moderate exercise (30 minutes 5 times a week) has been shown to reduce new diabetes cases by 58% over a 3-year period. By contrast, the drug metformin, which boosts insulin sensitivity, reduced new cases by only 31%.¹²⁷ The National Institutes of Health (NIH) is conducting a 12-year, 5000 patient study to further test the additive effects of diet and exercise on diabetes.

Several types of OHDs are available, including the following:

1. OHDs used to stimulate islet cells to increase endogenous insulin secretion and enhance insulin-receptor binding (sulfonylureas).

2. OHDs that act by slowing the digestion of sugars in the intestine (acarbose).

3. OHDs referred to as insulin-resistance reducers or “insulin sensitizers” (thiazolidinediones such as pioglitazone [Actos] and rosiglitazone [Avandia]). Insulin sensitizers improve the action of liver, muscles, and fat tissues and do not cause liver problems as seen with troglitazone (Rezulin), which was removed from the market in March 2000.

4. OHDs used to improve hepatic and peripheral tissue sensitivity to insulin (metformin [Glucophage]), thereby increasing the effectiveness of insulin found in the body.

The advantage of this last OHD is that it does not stimulate activity with concomitant weight gain. However, diarrhea develops for 2 to 3 weeks in approximately one-third of people using this drug. One potentially serious but rare side effect is lactic acidosis, a life-threatening buildup of lactic acid in the blood. This condition can be fatal in people with kidney or liver disease or alcoholism. The main clinical feature of lactic acidosis is hyperventilation.

Treatment of Long-Term Complications.: Prevention of long-term complications is the goal for all clients with DM. Risk of complications is associated independently and additively with hyperglycemia and hypertension. Intensive treatment of both these risk factors is required to prevent and minimize the incidence of most complications.²³⁷

Medical treatment of long-term diabetic complications may include dialysis or kidney transplantation for renal failure and vascular surgery for large vessel disease. Currently, the American Diabetes Association advises that people with diabetes take low-dose aspirin (75 to 162 mg) daily to help minimize risks such as heart attacks and strokes. Prophylactic aspirin therapy is recommended in both men and women with diabetes who are 40 years and older, although some diabetologists suggest that aspirin prophylaxis should begin at age 30.⁴¹

New treatment guidelines from the American College of Physicians recommend the use of statins (cholesterol-lowering drugs such as Crestor, Lipitor, Zocor, Mevacor, or Pravachol) for anyone with diabetes and diagnosed CAD—even if their cholesterol levels are normal.

Review of available data shows that statins reduced heart attacks and strokes by 22% to 44% in people with diabetes.²³¹ People with diabetes and normal cholesterol who have other cardiac risk factors, such as hypertension, obesity, smoking, age over 55, and chronic physical inactivity, may benefit from a nonstatin cholesterol medication such as gemfibrozil (Lopid).

Diabetic Ulcers.: The therapist often is involved in prevention and wound care for diabetic ulcers, which may help prevent amputation. Early recognition and prompt management of wounds, ulceration, and Charcot foot can facilitate healing. For example, a CDC study showed that people with diabetes who wore proper shoe protection had only a 20% recurrence rate of ulceration compared with an 80% rate for those without offloading.²³²

Offloading or pressure reduction is a key component for healing ulcers and preventing recurrence. The normal response to damaged areas is to spare them from pressure because they are painful. However, in the insensitive foot of a person with diabetes, this normal alteration of weight-bearing surface, pressure, and duration does not take place, resulting in repetitive stress and injury with subcutaneous and cutaneous necrosis and skin breakdown.

A marked improvement in the rate of healing for plantar ulcers has been reported using a combination of total-contact cast (TCC) and tendo-Achilles lengthening (TAL; percutaneous heel cord lengthening), as opposed to TCC alone.^{10,143,172,211}

The results of at least one study show TAL should not be done in anyone with complete anesthesia of the heel pad; increased dorsiflexion can increase the risk of heel ulceration. This procedure is advised only in a multidisciplinary setting able to provide adequate nutrition, wound care, surveillance, treatment of complications and other biomechanical abnormalities and intervene early in any developing ulcerations.¹⁰⁶

Other interventions include debridement, infection control, protective dressings, revascularization, proper nutrition, and client education. Active dressings, such as growth factors and living skin, are also in use. Topical application of growth factors on wounds without infection and with at least a minimal level of vascularization was introduced in the early 1990s and has progressed to include new techniques in skin transplantation (see the section on Skin Transplantation in Chapter 21).

Infrared light therapy, such as monochromatic near-infrared photo energy (MIRE), has been applied using the anodyne therapy system (ATS) to improve sensory impairment, reduce pain, and prevent and heal ulcers. When used in conjunction with other physical therapy interventions, MIRE has been shown to improve balance in clients with diabetic peripheral neuropathy. ATS has been shown to be effective in reversing the loss of protective sensation by improving circulation. Light absorbed by hemoglobin in the blood causes the release of nitric oxide, resulting in vasodilation and improved collateral circulation. Long-term studies are still needed to show whether the results can be sustained.^{128,129,140,198}

The use of cool laser therapy as a revascularization therapy is now available. Cool laser revascularization for peripheral artery therapy (CliRpath) uses a cool excimer laser and catheter system to vaporize arterial blockages, restoring blood flow and promoting wound healing. Reduction in pain, improved circulation, and facilitation of wound healing may help prevent limb loss in this population.

Treatment of diabetic peripheral neuropathic pain (DPNP) has not been successful using any one single intervention technique. The ideal treatment is correcting the underlying condition of chronic hyperglycemia. Many methods have been employed (e.g., capsaicin topical cream, acupuncture, and electrical stimulation) to address the painful symptoms of DPNP with limited and variable results. Medications aimed at chronic neuropathic pain have included tricyclic antidepressants (e.g., amitriptyline, nortriptyline, or imipramine), but anticholinergic effects, such as dry mouth, blurred vision, constipation, cardiac arrhythmias, and orthostatic hypotension, often limit their use.

More recently, off-label use of anticonvulsants, such as gabapentin (Neurontin) and pregabalin (Lyrica), have met with greater success. Serotonin-norepinephrine reuptake inhibitors, such as duloxetine (Cymbalta), can be used by some individuals to treat painful DPNP. By inhibiting the reuptake of these neurotransmitters, descending inhibitory pathways in the spinal cord are activated and block ascending pain signals to the brain.²⁵⁴

Transplantation.: Research is being conducted on the use of transplanted pancreatic islet cells rather than the entire pancreas. The transplant recipient receives one or more infusions of pancreatic islet cells that include insulin-producing beta-cells. Almost 500 people with type 1 diabetes have received islet transplants at 43 institutions worldwide in the last 5 years.²²²

High rates of insulin independence have been reported at 1 year in the leading islet transplant centers. Loss of insulin independence by 5 years occurs in the majority of recipients. Life-long immunosuppression and its complications limit this treatment to candidates who have the most severe, unstable glycemic control despite optimal insulin therapy.²²²

Stem cell research may find a way for people to use their own stem cells to develop them into islet cells and allow infusions without cell-rejection complications and the need for life-long immunosuppression. In addition, artificial pancreata provide hope for future treatment without repeated injections for the person with type 1 diabetes. An artificial pancreas contains a reservoir for insulin (which must be filled by the affected individual, typically through a tube in the abdomen), and an internal glucose monitor that continuously determines the plasma glucose level, automatically releasing the appropriate amount of insulin. Such instruments are expected to reach the market shortly. The use of wireless communication between a continuous glucose sampling device and an insulin pump would give people with diabetes a closed-loop system or electromechanical artificial pancreas.⁶³

PROGNOSIS.

Diabetes control depends on the proper interaction between the following three factors: (1) food, (2) insulin or oral medication to lower blood glucose, and (3) activity (e.g., sedentary or exertional) or exercise. When diabetes is regulated successfully, complications of hyperglycemia and hypoglycemia can be avoided with minimal disruption to a normal lifestyle. However, diabetes can be fatal even with medical treatment, or it can cause major permanent disabilities and seriously impair functional abilities. Studies have shown that type 2 DM raises a person’s risk of dying from heart disease by 2 to 3 times.²³⁴ In fact, about 50% of myocardial infarctions and 75% of strokes are attributable to diabetes. Diabetes is the leading cause of new blindness and is a contributory cause to renal failure and peripheral vascular disease.

Regardless of the modality of treatment used for the person with type 1 or type 2 DM, recent studies have shown clearly that tight glucose control (plasma glucose levels consistently within normal limits, approximately 100 mg/dl) delays onset and progression of diabetic complications. The only apparent danger in maintenance of tight control is the greater possibility of hypoglycemia, particularly in those people with type 1 DM who receive frequent exogenous insulin administration.⁴¹

11-16 SPECIAL IMPLICATIONS FOR THE THERAPIST

Diabetes Mellitus

PREFERRED PRACTICE PATTERNS

4C:

Impaired Muscle Performance

4J:

Impaired Motor Function, Muscle Performance, Range of Motion, Gait, Locomotion, and Balance Associated with Amputation

5G:

Impaired Motor Function and Sensory Integrity Associated with Acute or Chronic Polyneuropathies

6A:

Primary Prevention/Risk Reduction for Cardiovascular/Pulmonary Disorders

6B:

Impaired Aerobic Capacity/Endurance Associated with Deconditioning

7A:

Primary Prevention/Risk Reduction for Integumentary Disorders

7B:

Impaired Integumentary Integrity Associated with Superficial Skin Involvement

Client education is the key to therapeutic, nonsurgical treatment of the neuromusculoskeletal complications associated with diabetes. Extensive self-management is the focus of the educational program.^*

Exercise is a key component of the overall intervention plan.⁴¹ The client must be taught the importance of assessing glucose levels before and after exercise and to judge what carbohydrate and insulin requirements are suitable for the activity or workout. People with diabetes and peripheral neuropathy have a high incidence of injuries (e.g., falls, fractures, sprains, cuts, and bruises) during walking or standing and a low level of perceived safety. Suggested strategies for appropriate clinical intervention to reduce these complications are available.

Complications of Insulin Therapy

HYPOGLYCEMIA

Insulin therapy can result in hypoglycemia (low blood glucose, also called an insulin reaction)⁴⁸; tissue hypertrophy, atrophy, or both, at the site of injection; insulin allergy; erratic insulin action; and insulin resistance. Symptoms of hypoglycemia are related to two body responses: increased sympathetic activity and deprivation of CNS glucose supply (Table 11-16). The clinical picture may be varied from a report of headache and weakness to irritability and lack of muscular coordination (much like drunkenness) to apprehension, inability to respond to verbal commands, and psychosis.

Table 11-16

Clinical Signs and Symptoms of Hypoglycemia

Sympathetic Activity (Increased Epinephrine)	CNS Activity (Decreased Glucose to Brain)
Pallor	Headache
Perspiration^*	Blurred vision
Piloerection (erection of the hair)	Thickened speech
Increased heart rate (tachycardia)	Numbness of the lips and tongue
Heart palpitation	Confusion
Nervousness^* and irritability	Emotional lability
Weakness^*	Convulsion^*
Shakiness/trembling	Coma
Hunger

CNS, Central nervous system.

^*Signs most often reported by clients.

From Black JM, Matassarin-Jacobs E: Medical-surgical nursing, ed 5, Philadelphia, 1997, WB Saunders.

Symptoms can occur when the blood glucose level drops to 70 mg/dl or less, although this value varies among those with diabetes and can be lower than 70 mg/dl before symptoms are elicited. In diabetes, an overdose of insulin, late or skipped meals, or overexertion in exercise may cause hypoglycemic reactions. Immediately provide carbohydrates in some form (e.g., fruit juice, honey, hard candy, or commercially available glucose tablets or gel); a blood glucose test should be performed as soon as the symptoms are recognized. The unconscious person needs immediate medical attention; to prevent aspiration, fluids should not be forced. Hospitalization is recommended when the following occur:

• The blood glucose is less than 50 mg/dl and/or the treatment of hypoglycemia has not resulted in prompt recovery of altered mental status.

• The individual has had seizures or is unconsciousness.

• A responsible adult cannot be with the person for the next 12 hours.

• A sulfonylurea drug causes the hypoglycemia; this type of drug reduces liver conversion of glycogen to glucose and prolongs the period of hypoglycemia.

It is important to note that clients can exhibit signs and symptoms of hypoglycemia when their elevated blood glucose level drops rapidly to a level that is still elevated (e.g., 400 to 200 mg/dl). The rapidity of the drop is the stimulus for sympathetic activity–based symptoms; even though a blood glucose level appears elevated, affected individuals may still have symptoms of hypoglycemia.

When a person with diabetes mentions the presence of nightmares, unexplained sweating, and/or headache causing sleep disturbances, hypoglycemia may be indicated during nighttime sleep (most often related to the use of intermediate and long-acting insulins given more than once a day). These symptoms should be reported to the physician.

Erratic insulin action (i.e., low blood glucose followed by high blood glucose) can occur as a result of a variety of factors such as overeating, irregular meals, irregular exercise, irregular rest periods, chronic overdosage of insulin (Somogyi effect), emotional or psychologic stress, failure to administer insulin, or intermittent use of hyperglycemic or hypoglycemic drugs (e.g., aspirin, phenylbutazone, steroids, birth control pills, or alcohol).

The Somogyi effect occurs when the blood glucose level decreases to the point at which stress hormones (epinephrine, growth hormone, and corticosteroids) are released, causing a rebound hyperglycemia. Treatment consists of increasing the amount of food eaten and/or decreasing the insulin. The therapist may be a helpful source of education to help clients remember the many factors affecting their condition.

LIPOGENIC EFFECT OF INSULIN

Frequent injections of insulin at the same site can cause thickening of the subcutaneous tissues (hypertrophy or lipohypertrophy) and a loss of subcutaneous fat (atrophy or lipoatrophy), resulting in a dimpling of the skin that is lumpy and hard or spongy and soft. These abnormal tissue changes may cause decreased absorption of the injected insulin and poor glucose control.

The client usually is instructed to choose an injection site that is easily accessible (e.g., thighs, upper arms, abdomen, or lower back) and relatively insensitive to pain (away from the midline of the body). Sites of injection should be rotated, and rotation within each area is recommended. An individual can rotate within an area using 1 inch of the surrounding tissue at a time. The client who is going to exercise should avoid injecting sites or muscles that will be exercised heavily that day because exercise increases the rate of absorption. Following a definite injection plan can help avoid tissue damage.

Even with an insulin pump the infusion site should be changed every 2 or 3 days or whenever the client’s blood glucose is above 240 mg/dl for two tests in a row. Rotating insertion sites will help prevent infection and tissue damage.

DIABETIC KETOACIDOSIS

The therapist must always be alert for signs of ketoacidosis (e.g., acetone breath, dehydration, weak and rapid pulse, and Kussmaul’s respirations) progressing to hyperosmolar coma (polyuria, thirst, neurologic abnormalities, and stupor). Immediate medical care is essential. If it is not clear whether the symptoms are the result of hypoglycemia or hyperglycemia (Table 11-17), the health care worker is advised to administer fruit juice or honey. This procedure does not harm the hyperglycemic person but could potentially save the hypoglycemic person. Everyone with diabetes should wear a medical alert identification tag.

Table 11-17

Comparison of Manifestations of Hypoglycemia and Hyperglycemia

Variable	Hypoglycemia	Hyperglycemia
Onset	Rapid (minutes)	Gradual (days)
Mood	Labile, irritable, nervous, weepy	Lethargic
Mental status	Difficulty concentrating, speaking, focusing, coordinating	Dulled sensorium, confused
Inward feeling	Shaky, hungry, headache, dizziness	Thirst, weakness, nausea/vomiting, abdominal pain
Skin	Pallor, sweating	Flushed, signs of dehydration (see Box 5-6)
Mucous membranes	Normal	Dry, crusty
Respirations	Shallow	Deep, rapid (Kussmaul’s respirations)
Pulse	Tachycardia	Less rapid, weak
Breath odor	Normal	Fruity, acetone
Neurologic	Tremors; late: dilated pupils, seizures	Diminished reflexes, paresthesias
Blood Values
Glucose	Low <50 mg/dl	High ≥250 mg/dl
Ketones	Negative	High/large
pH	Normal	Low ≤7.25
Hematocrit	Normal	High
Urine Values
Output	Normal	Polyuria (early) to oliguria (late)
Glucose	Negative	High
Ketones	Negative/trace	High

From Ignativicius D, Workman M, et al: Medical-surgical nursing across the health care continuum, ed 3, Philadelphia, 1999, WB Saunders.

VITAMIN B DEFICIENCY

Some individuals using Metformin can develop vitamin B12 deficiency resulting in serious damage to the nervous system. Complications can be minimized with early detection and intervention. Anyone on Metformin, especially high doses or a prolonged course of therapy, should be screened for the deficiency. The therapist can help monitor this with the client and recognize any early neurologic signs and symptoms.²⁴⁴

Diabetes and Exercise

An overwhelming body of evidence now exists that acute muscle contractile activity and chronic exercise improve skeletal muscle glucose transport and whole-body glucose homeostasis in the person with type 2 DM (Box 11-6).²²⁴ Exercise helps to increase insulin sensitivity, thus lowering blood glucose levels. Increased insulin sensitivity allows the body to utilize the available blood glucose for the person with type 2 diabetes; an increase in insulin sensitivity can last 12 to 72 hours after exercise.

Box 11-6 DIABETES MELLITUS: KEY POINTS TO REMEMBER

General Guidelines

• Although “safe” blood glucose levels are between 100 and 250 mg/dl (i.e., the person is not likely to experience DKA), the goal of therapy may be toward tighter control (e.g., in a young person with type 1 DM, 90 to 130 mg/dl) or moderate control (e.g., in an adult with type 2 DM, up to 150 mg/dl). A measurement more than 120 mg/dl should still be monitored closely in any age group

• If the blood glucose level is ≤100 mg/dl, a carbohydrate snack should be given and the glucose retested in 15 min to ensure an appropriate level. Food eaten in response to blood glucose levels between 70 and 100 mg/dl is symptom dependent (i.e., if a person’s blood glucose is 80 mg/dl but no signs or symptoms of hypoglycemia are present, no snack is necessary)

• Observe carefully for signs or symptoms of DKA: acetone breath, dehydration, weak and rapid pulse, Kussmaul’s respirations

• Avoid exercise if blood glucose ≥250 mg/dl with evidence of ketosis

• Administer fruit juice or honey to anyone with diabetes who is in a hypoglycemic state. If uncertain whether the person is hypoglycemic or hyperglycemic, provide juice or honey anyway

• Exercise must be carefully planned in conjunction with food intake and administration of insulin or oral hyperglycemic agents

• Do not exercise during peak insulin times. The peak activity of insulin occurs at different times depending on the type, dose, and time of the insulin injection (see explanation in text)

• When under stress, the person with diabetes has increased insulin requirements and may become symptomatic even though the disease is usually well-controlled in normal circumstances

• Avoid exercising late at night if this has not been gradually and consistently incorporated into the overall lifestyle. Delayed hypoglycemic reactions can occur during sleep hours after heavy, unaccustomed exercise late in the evening

Before Exercise

• Take at least 17 oz of fluid before exercise (approximately two 8 oz glasses).

• Glucose levels must be monitored immediately before exercise.

• Do not exercise when blood glucose levels are at or near 250 mg/dl with urinary ketones and use caution if glucose level is >300 mg/dl and no ketosis is present.²⁷¹

• Do not exercise without eating at least 2 hr before exercise (exercise about 1 hr after a meal is best, but individual variations must be determined).

• Do not inject short-acting insulin in muscles or sites close to areas involved in exercise within 1 hr of exercise because insulin is absorbed much more quickly in an active extremity.

• Clients with type 1 DM may have to reduce the insulin dose or increase food intake when initiating an exercise program.

• Ketosis can be checked by means of a urine test before exercise (e.g., if the blood glucose is close to 250 mg/dl). If the test is positive (i.e., showing large numbers of ketones in the urine), exercise should be delayed until the urine test shows negative or low numbers of ketones. The person should administer insulin. Delay exercise until glucose and ketones are under control.

• Do not use drugs that may contribute to exercise-induced hypoglycemia (e.g., β-blockers, alcoholic beverages, diuretics, estrogens, phenytoin).

• Menstruating women need to increase their insulin during menses, especially those who are inactive or who do not exercise on a regular basis

During Exercise

• It is best to exercise regularly (5 times/wk or at least every other day) and consistently at the same time each day.

• Duration of exercise is optimal at 40 to 60 min, although as little as 20 to 30 min of continuous aerobic exercise is beneficial in improving glucose homeostasis.

• During prolonged activities, a readily absorbable carbohydrate snack (e.g., fruit) is recommended for each 30 minutes of activity. After exercise, a more slowly absorbed carbohydrate snack (e.g., bread, pasta, crackers) helps prevent delayed-onset hypoglycemia. Activities should be stopped with the development of any symptoms of hypoglycemia, and blood glucose tested.

• Replace fluid losses adequately.

• Monitor blood glucose every 30 min during prolonged exercise.

• Anyone with diabetes should not exercise alone. Health care workers, partners, teammates, and coaches must understand the possibility of hypoglycemia and how to manage it.

After Exercise

• Glucose levels must be monitored 15 min after exercise, especially if exercise is not consistent.

• Increase caloric intake for 12 to 24 hr after activity, according to intensity and duration of exercise.

• Reduce insulin, which peaks in the evening or night, according to intensity and duration of exercise.

DKA, Diabetic ketoacidosis; DM, diabetes mellitus.

There is a high prevalence of people with underlying skeletal muscle insulin resistance or impaired skeletal muscle glucose disposal such as occurs with inactivity, bed rest, limb immobilization, or denervation. Therapists must recognize, understand, and use the role of skeletal muscle in glucose homeostasis to address the needs of clients with any of these risk factors. Sinacore and Gulve published an excellent, detailed review of the pathways of glucose transport into skeletal muscle and the pathophysiology of insulin action in skeletal muscle as it contributes to disturbances of whole-body glucose metabolism.²²⁸

A program of planned exercise, including all the elements of fitness (flexibility, muscle strength, and cardiovascular endurance) can benefit persons with diabetes, especially those with type 2 DM. Exercise increases carbohydrate metabolism (which lowers the blood glucose level); aids in maintaining optimal body weight; increases high-density lipoproteins (HDLs); and decreases triglycerides, blood pressure, and stress and tension (Table 11-18).

Table 11-18

Benefits and Potential Risks of Exercise in People with Diabetes Mellitus

^*These are potential risks over the long term. In general, the benefits of regular exercise outweigh the risks. DM, Diabetes mellitus.

^†Not confirmed for insulin-dependent diabetes mellitus (type 1 DM).

Exercise and physical activity (even leisure-time physical activity and activity on the job) have been shown to independently reduce the risk of total and cardiovascular mortality of adults with type 2 diabetes. Exercise capacity is reduced by diabetes-related CVD, but exercise training is an excellent therapeutic adjunct in the treatment of diabetic CVD.¹⁶¹

The favorable association of physical activity with longevity occurs regardless of BMI, blood pressure, smoking habits, and total cholesterol levels.^108,109 Once again, the therapist can be very instrumental in client education on the importance of exercise for a wide range of reasons and benefits to the individual with diabetes.

GENERAL EXERCISE CONSIDERATIONS

For anyone with diabetes, type 1 or type 2, the exercise prescription must take into account any of the complications present, especially cardiovascular changes, autonomic and sensory neuropathy, and retinopathy.²⁷¹ Muscle damage, with accompanying insulin resistance and impaired glucose uptake and disposal, can occur when untrained individuals begin to exercise.²²⁸ For this reason, clients with diabetes must start any new activity at a well-tolerated intensity level and duration, gradually increasing over a period of weeks or even months.²⁷¹

Some thought should be given to the specific type of exercise selected. The young individual, in good metabolic control, can safely participate in most activities. The therapist should always be aware of and screen for clients who may have eating disorders, especially those who engage in excessive, intense exercise as a means of controlling their weight. Specific screening methods and questions are available for the therapist.⁹⁰

The middle-aged and older person with diabetes should be encouraged to be physically active, but because the aging process leads to degeneration of musculoskeletal structures, exercise can exacerbate these problems.⁴¹

However, even for the person with type 1 DM in good control, sports in which hypoglycemia may be life-threatening (e.g., scuba diving, rock climbing, or parachuting) should be discouraged. Walking necessitates care toward proper footwear for the person who does not already have evidence of peripheral neuropathy.

Intermittent, high intensity activities (e.g., racquetball, baseball) or contact sports (e.g., basketball or soccer) should be avoided to prevent trauma (especially to the feet or eyes). High resistance strength-training programs should be limited to the young person with diabetes who has no diabetic complications. More specific recommendations for the long-distance runner and other athletes are available.^{4,15,144,159,243}

Low-resistance strength training programs should be encouraged unless retinopathy is present (weightlifting is contraindicated in anyone with proliferative retinopathy; see Box 11-7). Exercise involving jarring or rapid head motion may precipitate hemorrhage or retinal detachment. Outdoor activities must be evaluated carefully, taking into consideration the weather extremes (hot or cold) and the person’s ability to maintain distal circulation. Stationary indoor equipment (many types are now available) may be the best overall choice.

Box 11-7 CONTRAINDICATIONS TO EXERCISE IN DIABETES MELLITUS

• Poor control of blood glucose levels

• Unevaluated or poorly controlled associated conditions:

• Retinopathy

• Hypertension

• Neuropathy (autonomic or peripheral)

• Nephropathy

• Recent photocoagulation or surgery for retinopathy

• Dehydration

• Extreme environmental temperatures (hot or cold)

EXERCISE PRECAUTIONS

As positive as exercise is in the prevention and control of diabetes, the therapist must keep in mind that diabetes is a metabolic disorder with cardiovascular and circulatory implications. Reduced blood flow to the skin and skeletal muscle can be further compromised by intense exercise, and recovery time is longer. All possible effects of exercise must be kept in mind when designing an exercise program. Strenuous exercise can have some serious side effects and is not recommended for most people with diabetes.¹⁹⁰

Before beginning any exercise program, the person with diabetes should undergo a detailed medical evaluation with appropriate diagnostic studies. Screening should be done for the presence of macrovascular and microvascular complications that may be worsened by the exercise program. A careful history and physical examination should be done by the physician and should focus on the signs and symptoms of disease affecting the heart, blood vessels, eyes, kidneys, and nervous system.^41,271

The therapist can help by designing an exercise program that suits the individual’s needs. Low-impact activities, such as walking, bicycling, and swimming, are good choices for anyone who has a loss of sensation in the feet. Strength training, especially upper body work, puts no additional strain on the feet. Resistance exercise training may help avoid insulin therapy, especially for overweight women with gestational DM.²⁵ Moderate intensity resistive training also can improve mobility and strength in older adults with diabetes, potentially reducing the rate of mobility loss during aging.²⁴

DIABETIC AUTONOMIC NEUROPATHY

Many people with diabetes may not be able to exercise intensely to a calculated heart rate because of preexisting heart conditions, deconditioning, age, neuropathies, arthritis, or other joint problems. Exercise may be contraindicated in anyone with a severe form of autonomic neuropathy (Box 11-7), especially anyone with vasomotor instability, angina, and a history of myocardial infarction.⁴¹ The therapist is advised to communicate and collaborate with the client and physician when considering an exercise program for anyone with this problem.

Generally, individuals with autonomic neuropathy have a poor ability to perform aerobic exercise because of decreased maximal heart rate and increased resting heart rate. Persons with a generalized form of autonomic neuropathy may have hypotensive episodes after exercising, especially those who are deconditioned. They also demonstrate a predisposition toward dehydration in the heat and poor exercise tolerance in cold environments.

People with diabetic autonomic neuropathy may have a higher resting heart rate but lower maximal heart rate, making exercise at safe levels more difficult. It may be better to use the percent of heart rate reserve (% HRR), which is the difference between resting heart rate and maximum heart rate, as a valid measure in prescribing exercise intensity instead of the rating of perceived exertion (RPE) scale, which relies on self-assessment of exertion.⁴² The American College of Sports Medicine (ACSM) recommends exercise intensity levels for clients with diabetic autonomic neuropathy should remain in the 40% to 75% HRR span.³

Some people with autonomic neuropathy may have silent myocardial infarctions without angina. The first symptom may be shortness of breath resulting from congestive heart failure. Decrease in nerve innervation to the heart associated with this type of neuropathy may prevent a normal increase in heart rate with stress or exercise, requiring careful observation and monitoring of vital signs during exercise. Blood pressure regulation is altered with autonomic neuropathy; exercise can further stress the impaired system. Clients with autonomic neuropathy are prone to hypothermia, dehydration, and hypotension or hypertension.

Diabetes is associated with reduced tolerance to heat. Autonomic neuropathy may also include changes in thermoregulation with a decreased or altered ability to perspire. Exercise with a concomitant increase in core body temperature can lead to heat stroke.¹⁹² Impairment of sweating has been demonstrated even with isometric exercise.¹⁹⁴ Proper hydration is essential, and precautions should be taken to avoid heat stroke. The Valsalva maneuver should be avoided.

EXERCISE IN TYPE 1 DIABETES MELLITUS

The person with type 1 DM tends to be thin, may be poorly nourished, and because of the islet cell deficiency, always needs exogenous insulin for adequate control of blood glucose. Exercise can increase strength and facilitate maintenance of weight and provide other important benefits (see Table 11-18), but unfortunately exercise has not been proven to provide increased glycemic control for the person with type 1 DM.

During exercise in individuals without diabetes, blood glucose levels remain normal, largely as a result of hormonal mediation with an increase in glucagon and catecholamines, which supply the necessary glucose for use by muscles and other body tissues. In a person with type 1 DM, these hormonal adaptations are lost and as a consequence, when too little insulin is available, the cells are sensing starvation so an excessive release of glucagon and catecholamines occurs.

These hormones further increase glucose mobilization into the bloodstream and significantly increase an already high level of glucose and ketones. If the hyperglycemia and ketosis is high enough and/or if the person is dehydrated, DKA can be precipitated.⁴¹

The person with well-controlled type 1 DM may commonly work out for approximately 30 to 45 minutes of sustained intense aerobic exercise without problems. Lack of adequate glycogen stores (i.e., decreased glycogen stores in the liver and to a lesser extent, in skeletal muscle) leads to impaired aerobic exercise endurance when compared with the nondiabetic person.

Hypoglycemia is a common occurrence in persons with type 1 DM who are exercising. In those who do not have diabetes, plasma insulin levels decrease during exercise and insulin counterregulatory hormones (glucagon and epinephrine) promote increased hepatic glucose production, which matches the amount of glucose used during exercise.

For the person with type 1 DM, who is not insulin deficient (because of exogenous administration of insulin), plasma insulin concentrations may not fall during exercise and may even increase if exercise occurs within 1 hour of insulin injection. These sustained insulin levels during exercise enhance peripheral glucose uptake and stimulate glucose oxidation by exercising muscle. For this reason, insulin should not be injected into muscles or at sites close to areas involved in exercise within 1 hour of exercise. Insulin pump infusion sites must be subcutaneous and not intramuscular.

Moderate periods of exercise provide beneficial effects, but longer periods may result in hypoglycemia. Watch for symptoms such as sweating, shakiness, nausea, headache, and difficulty concentrating. The greatest risk of severe hypoglycemia occurs 6 to 14 hours after strenuous exercise. Muscle and hepatic glycogen must be restored during periods of rest. Insulin and caloric intake must be adjusted after strenuous exercise to avoid severe nocturnal hypoglycemia.

EXERCISE IN TYPE 2 DIABETES MELLITUS

In contrast, people with type 2 DM are often obese, and exercise is a major contributor in controlling hyperglycemia. Exercise can improve short-term insulin sensitivity and reduce insulin resistance, making it possible to prevent type 2 DM in those persons at risk and to improve glycemic control in those with diabetes.²²⁴ These effects disappear a few days after exercise is discontinued. Long-term higher intensity exercise training (80% peak aerobic capacity) provides more enduring benefits to insulin action compared to low or moderate intensity exercise.⁵⁷

Hypoglycemia is not as common a problem for the person with type 2 DM because endogenous insulin levels usually can be maintained. Control of blood glucose levels by lowering the medication dose or increasing carbohydrate intake (or both) before exercise can prevent hypoglycemia. However, individuals with type 2 diabetes who receive insulin or sulfonylureas may have a risk for hypoglycemia similar to that of people with type 1 DM.^41,224

For anyone with diabetes, exercise should not be initiated if the blood glucose is 70 or less. Since one effect of exercise is the transfer of glucose in the cells, glucose levels should be checked again 2 hours after exercise. Vigorous exercise should not be undertaken within 2 hours before going to sleep at night because this is when exercise-induced hypoglycemia can occur with potentially fatal consequences.

Unplanned exercise can be dangerous for people taking insulin or oral hypoglycemic agents. During periods of exercise, muscles are stimulated to take up glucose to supply the fuel to the working muscles, causing blood glucose levels to fall abruptly. However, anyone with blood glucose levels at or near 300 mg/dl should NOT exercise because vigorous activity also can raise the blood glucose level by releasing stored glycogen. Exercise or therapy sessions should be scheduled to avoid peak insulin times (see Table 11-15) and to avoid periods of fasting (e.g., missed meal or just before the next meal).

Exercise in the morning is recommended to avoid hypoglycemia resulting from fluctuations in insulin sensitivity caused by factors such as diurnal variations in growth hormone. Growth hormone levels remain low in the afternoon, and less gluconeogenesis occurs. Vigorous or intense exercise late in the day or evening can lead to delayed hypoglycemia during sleep, which is dangerous.

BALANCING INSULIN, FOOD, AND EXERCISE

As mentioned, insulin should be injected in sites away from the part of the body involved in exercising. Because glucose can enter the cells without insulin during exercise, food should be eaten if the person is exercising more than usual. Conversely, when exercising less often, a lighter diet or more insulin is required.

Glucose levels should be monitored before and after exercise (or therapy activities), remembering that the effect of exercise can be felt up to 12 to 24 hours later. Those clients taking insulin should have their own glucose monitoring devices (fingerstick or laser punctures).

After exercise, available glucose is important for the replenishment of muscle glycogen stores. Bouts of hypoglycemia can be delayed until hours after completion of exercise. The insulin-dependent person must regulate activity so that the rate of energy expenditure balances the amount and type of insulin and food intake (Table 11-19). Women who are menstruating may need to increase their insulin during menses.

Table 11-19

Making Food Adjustments for Exercise: General Guidelines

^*100 mg/dl = 100 ml. The 100 mg/dl is a general guideline. Wide individual variations occur in this area. The timing of food intake may be symptom-dependent. Some individuals may experience symptoms of hypoglycemia when the blood glucose is 150 mg/dl, others not until the level is below 80 mg/dl and so on.

EXERCISE AND THE INSULIN PUMP

The normal metabolic response to exercise in a person who does not have diabetes is to decrease the release of insulin as muscles contract, causing the transport of more blood glucose into cells without insulin. A small amount of circulating insulin remains available during exercise to counterbalance the release of glucose-raising hormones (e.g., catecholamines, glucagon, growth hormone, and cortisol).

CSII therapy brings the exercising individual with diabetes a response as close to normal as possible. But anyone with diabetes who uses an insulin pump must make frequent insulin adjustments to mimic the normal metabolic response, thereby maintaining a more normal glycemic control, especially during periods of higher intensity or longer duration exercise.⁴³ Most people using an insulin pump have type 1 (insulin-dependent) DM, although anyone with type 2 DM who uses insulin can also wear a pump.

Time of day, exercise intensity, and elevated starting blood glucose levels appear to affect the metabolic response and can result in hyperglycemia instead of the more usual hypoglycemia for several hours after exercise. Metabolic control can deteriorate with intense exercise even in people who have tightly controlled blood glucose levels. It is suggested that 30 minutes of mild-to-moderate exercise is possible 2 or 3 hours after breakfast when using insulin pumps. The insulin level can be adjusted to minimize circulating free insulin levels and the risk of hypoglycemia during and after activity.^43,235

One of the disadvantages of an insulin pump is that it can malfunction or become displaced without the person knowing it. Exercise can exacerbate the situation when insulin delivery has been unknowingly disrupted and hypoinsulinemia is developing. The therapist should always be alert to any signs of DKA in clients using an insulin pump. Teach the client to be vigilant during exercise to maintain the integrity of the infusion site and to pay attention to any symptoms of impending DKA (e.g., thirst, nausea, weakness, or excessive urination).

Before the advent of the insulin pump, anyone with type 1 diabetes whose blood glucose was less than 100 mg/dl was instructed to consume a carbohydrate snack before starting or continuing the activity. With CSII, pump users can simply reduce or suspend insulin during the activity. Insulin reduction and carbohydrate intake are determined by the intensity and duration of the exercise activity. For example, a change in either insulin or carbohydrate intake may compensate for shorter, less intense activities but not in the case of intense, aerobic exercise.⁴³

Diabetes and Neuromusculoskeletal Complications

The treatment of musculoskeletal problems does not differ from treatment for these same conditions in the nondiabetic population. Early aggressive therapy for the adhesive capsulitis usually results in restoration of functional motion, even though full range of motion may not be achieved.

Hand function can be maintained and disease progression delayed with hand therapy, especially for the stiff hand syndrome. SLJM does not always benefit from therapy, but treatment intervention should be tried. For either of these conditions, the client must understand the importance of a self-directed exercise program established by the therapist to prevent recurrence of symptoms and to maintain functional outcomes.

Intervention for CTS must take into account the neuropathic and the entrapment components in the person with diabetes; surgical decompression may not be beneficial because of the neuropathic component. Nonsurgical efforts should be the focus of treatment. In conditions such as adhesive capsulitis and CRPS a successful outcome is more likely with early medical and therapeutic intervention.

Diabetes and Foot Care

Disorders of the feet constitute a source of increasing morbidity associated with diabetes. Foot problems are a leading cause of hospital admission in people with diabetes, and diabetes is the most common reason for lower limb amputation. Half of those cases are preventable with proper foot care.^229,256 Treatment of the underlying diabetes has little effect on any joint disease already present. The most beneficial intervention includes stabilizing the joint, minimizing trauma, maintaining muscular strength, and performing daily foot care.

The therapist must teach each person with diabetes proper foot and skin care (see Box 12-14). Regular foot checks after exercise using a mirror to inspect all surface areas and between the toes is advised. Having the therapist demonstrate and consistently carry this out with the client is a helpful educational tool. Any areas of warmth, erythema, swelling, or skin changes must be evaluated carefully and immediately. The therapist is advised to reinforce client education at each and every session.

DIABETIC PERIPHERAL NEUROPATHY

Assess for risk factors for amputation (e.g., previous ulcer or amputation) and for signs of diabetic neuropathy (e.g., numbness or pain in hands or feet or footdrop; see Table 12-21 and discussion of neuropathic [diabetic] ulcers). Scarborough²¹⁴ includes an excellent summary of assessment (tests and measures) for the foot and lower extremity. Vinik and Mehrabyan also offer an excellent review of diabetic neuropathies that will be of interest to any clinician working with this problem.²⁵⁶

Keep in mind that ankle-brachial index (ABI) measurements used to assess arterial circulation may have limited value in anyone with diabetes because calcification of the tibial and peroneal arteries may render them noncompressible.³⁰

Provide clients with a monofilament for self-testing (Fig. 11-15). For a description of an easy and reliable method to test for protective sensation using the Semmes-Weinstein monofilaments, see the reference section.^54,173 This test is an easily used clinical indicator for identifying people who are at risk for developing foot ulcers and requiring subsequent amputations. It can clearly demonstrate physiologic changes in peripheral nerve function. If the person cannot feel the monofilament when applied with slight pressure against the skin, there is an increased risk of ulceration. The results of this test provide a definitive idea of who can benefit most from preventive care, education, and prescription of appropriate therapeutic footwear.¹⁷³

Figure 11-15 Semmes-Weinstein monofilament testing for protective sensation. Performed if the client is suspected of having peripheral neuropathy or known diabetes with possible peripheral neuropathy. The 5.07 monofilament (calibrated to apply 10 grams of force) has been adopted for screening in the diabetic population. The monofilament is applied perpendicular to the test site with enough pressure to bend the monofilament for 1 second. Abnormal response: client does not perceive the monofilament. Do not test over calloused areas. An initial foot screen should be performed on anyone with diabetes and at least annually thereafter. Anyone who is at risk should be seen at least four times a year to check their feet and shoes to help prevent foot problems from occurring. (From Seidel HM: Mosby’s physical examination handbook, ed 6, St Louis, 2006, Mosby.)

Decreased sensation in the feet associated with diabetic neuropathy can affect both the timing and quality of gait, requiring retraining of the somatosensory and vestibular systems to help compensate for the somatosensory deficit.^101,193 Gait and strength training are important in the management of large-fiber neuropathies when impaired vibration, depressed tendon reflexes, and shortening of the Achilles tendon occur.²⁵⁶ Diabetes gait may occur independent of sensory impairment. Increased joint movement, wider stance, and slower pace demonstrated in some individuals with type 2 diabetes may be neurologic in origin and not related to muscle weakness or loss of sensation in the feet.¹⁹¹

Anyone with peripheral neuropathy is advised to avoid soaking the feet. There is a danger of burns, and prolonged exposure to warm water leaves the skin susceptible to fungal infections. Whirlpools are contraindicated and baths are not advised (showering may be best). Bathing and soaking remove the protective barrier from the skin and can lead to other infections, especially if there are fissures from dry skin caused by decreased circulation.

The first Consensus Guidelines for DPNP developed by the American Society of Pain Educators (ASPE) are now available.⁷ Having a standard of care is important in the treatment of pain associated with DPNP. Improved safety and quality of care may result in fewer amputations and potentially better compliance with recommendations for physical activity and exercise with subsequent decreased secondary complications associated with poor glycemic control.

NEUROPATHIC (DIABETIC) ULCERS

The most common cause for neuropathic (diabetic) ulcers is excessive plantar pressure in the presence of sensory neuropathy and foot deformity. Neuropathic foot ulcers can occur anywhere pressure or shear force is applied to the foot (top, sides, or bottom). Many occur beneath the metatarsal heads and are the result of painless trauma caused by excessive plantar pressures during walking.¹⁷⁴

The presence of corns or calluses is an indication that footwear fits poorly and should be carefully evaluated by the therapist. Additionally, cartilage requires insulin for glucose uptake, metabolism of carbon dioxide, and collagen synthesis. Lacking an adequate supply, the articular cartilage in the person with diabetes does not tolerate repetitive trauma, compression, and motion, making proper footwear all the more important.¹⁹⁷

Note the location of any foot ulcerations for possible causes that can be corrected. For example, ill-fitting shoes may cause ulcers on the medial or lateral borders of the feet, whereas ulcers on top of the foot may be caused by deformities such as hammer (claw) toes.

The risk of ulceration and poor wound healing in the diabetic population underscores the importance of therapists providing nonsurgical alternatives for these problems. Although the management of the diabetic foot (Charcot joint) sometimes requires surgery, most people can be treated with appropriate cast, shoe, orthotic devices, or other therapeutic footwear. When a neuropathic joint is detected early, offloading the joint and avoiding weight bearing for 8 weeks may prevent progression of disease.

The presence of a previous history of plantar ulceration may alert the therapist to the need to teach the client how to control activity levels to lessen shear forces on scars from previous ulcers.²⁷ Orthoses are often used to redistribute or move pressure away from a blister or other area of pressure. Soft, moldable orthoses are preferred to the rigid orthoses used by clients with other types of foot problems. An excellent review of various offloading techniques for the treatment of neuropathic ulcers is available.²²¹

TCC is an effective intervention for neuropathic plantar ulcers. Monitoring of foot problems through the use of skin temperature changes using dermal thermography may provide valuable information to the clinician in the detection, treatment, and prevention of neuropathic foot problems.¹¹

Total contact inserts (TCI) and metatarsal pads can be used to reduce excessive plantar stresses, thereby preventing skin breakdown and ulceration. The TCI reduces excessive pressures at the metatarsal heads by increasing the contact area of weight-bearing forces. Metatarsal pads act by compressing the soft tissues proximal to the metatarsal heads and relieving compression at the metatarsal heads.¹⁷⁴

The prevention of foot problems before they begin is always the most effective method in offsetting the development of foot ulceration and infection and their potentially devastating effects. The use of proper footwear, proper cleaning and lubrication of the feet, safe removal of corns or calluses, and the removal of mechanical sources of foot pressure are critical components in the prevention of foot problems. Client education is a key component in the monitoring and detection of potential difficulties.¹⁹⁷

DELAYED WOUND HEALING

Because wound healing (surgical and nonsurgical) is impaired in the diabetic foot, surgery can be accompanied by increased risks of poor healing and infection. Sympathectomy, arthrodesis, and joint immobilization have not been proved helpful. Organ transplantation in someone with diabetes is also a risk factor for delayed wound healing because of the chronic immunosuppression required.²²⁷

The detrimental effects of cigarette smoking on wound healing and peripheral circulation are well documented (see the section on Substance Abuse in Chapter 3). Smoking increases insulin resistance, worsens diabetes complications, and has a negative effect on prognosis. People with diabetes who smoke have a higher all-cause mortality rate than those who do not smoke.²³³

Smoking cessation is one of the two most important ways to reduce macrovascular complications in adults with diabetes. Control of hypertension is the other. The American Diabetes Association recommends that all health care providers routinely identify the smoking (tobacco use) status of clients with diabetes and offer cessation support and education.⁶

Substance abuse of any kind can impair or slow the rehabilitation process, especially delaying wound healing. Client education in this area is an important aspect of treatment. Despite strong evidence that clinician support of smoking cessation is effective for smokers who have diabetes, only about half report that their physician ever advised them to stop or cut down on their smoking (or substance use).¹⁵²

The U.S. Public Health Service Clinical Guideline²⁴⁵ suggests health care providers use the 5 As: ask, assess, advise, assist, and arrange. A brief nonconfrontational discussion of smoking cessation may help move the smoker to the next level of readiness. The clinician can help clients think about what will be better if they quit; moving the person to the contemplation stage (ready to quit in the next 6 months) doubles the chance of quitting during that time.¹⁹⁹

Diabetes and Physical Agents

Numerous studies from the 1980s and continued ongoing research have documented the large interindividual and intraindividual variability in subcutaneous insulin absorption, a major contributing factor in the variability of blood glucose. The therapist must be aware of these factors and plan intervention accordingly. Specifically, insulin absorption is impaired or altered by smoking, injection site, thickness of skinfold (adipose tissue), exercise, subcutaneous edema, local subcutaneous blood flow, ambient and skin temperature, and local massage.^9,103

The application of heat causes local vasodilation and hyperemia (excess blood to an area), necessitating burn precautions in this population. In a therapy practice, heat application may take the form of hot packs, paraffin, hydrotherapy, fluidotherapy, infrared radiation, ultrasound, or aquatic (pool) physical therapy.

Heat from the use of hot baths, whirlpools, saunas, or sun beds has been shown to accelerate the absorption of subcutaneous injections of insulin, by increasing skin blood flow. To reduce the risk of hypoglycemia, local application of heat to the site of a recent insulin injection should be avoided. The use of cryotherapy (cold) with its effects of vasoconstriction and decreased skin blood flow would be expected to slow or delay insulin absorption from the injection site.

Diabetes and Menopause

As life expectancy increases, women are living a greater proportion of their lives in the postmenopausal phase, a time when the prevalence of type 2 diabetes also increases. The therapist should be aware that the consequences of CVD, osteoporosis, and cancer are more pronounced in women who have type 1 or type 2 diabetes, especially in women who have metabolic syndrome followed by the development of type 2 diabetes.

The transition from premenopause to postmenopause estrogen-deficient status is associated with the emergence of many features of the metabolic syndrome, such as central obesity (intraabdominal body fat), insulin resistance, and dyslipidemia, which are also known to be risk factors for CVD. The prevalence of the metabolic syndrome increases with menopause and may partially explain the apparent acceleration of heart disease after menopause.³⁵

Women with type 1 diabetes frequently go through menopause at an earlier age than women who do not have diabetes. Premature or early menopause may be considered an unstudied complication of type 1 diabetes.⁵⁸ Risk factor assessment for any of these comorbidities throughout the life cycle is especially important for any woman who has diabetes.

As the woman with diabetes approaches menopause, changes in estrogen and progesterone affect how cells respond to insulin and therefore blood glucose levels. Menopause symptoms can mimic low blood glucose levels (e.g., moodiness or short-term memory loss).

Sleep disturbance and weight gain associated with menopause make it harder to control blood glucose levels. There is an increased risk of urinary tract infection, especially for the menopausal/postmenopausal woman on insulin and/or who has had diabetes for 10 or more years.²³ During the postmenopause years when female hormone levels remain low, insulin sensitivity may increase with a drop in the expected blood glucose levels.²⁰⁶

There are conflicting reports on the role of hormone replacement therapy (HRT) for postmenopausal women who have type 2 DM. Whether HRT improves glycemic control or worsens insulin sensitivity remains unproved. Results may vary according to the type of HRT, age of the woman, and route of administration.^91,122

Diabetes and Psychosocial Behavior

The therapist should keep in mind the psychologic and behavioral aspects of diabetes with regard to improving clinical outcomes. Common psychologic problems known to complicate diabetes management include poor self-esteem, impact on the family dynamics, family and social support, compliance and motivation, eating disorders, quality of life, and so on. A team approach that includes close collaboration between diabetologists, psychologists, and physical therapists is important.¹

Diabetes and Aquatic Physical Therapy³⁷

See also Appendix B: Guidelines for Aquatic Physical Therapy.

The Aquatics Section of the American Physical Therapy Association (APTA) has an annotated bibliography with relevant articles related to pool therapy, including the use of aquatics with medical conditions such as diabetes mellitus. This document is available through the Aquatics Section of the APTA.

Swimming may be a good choice to offer the individual with diabetes, once again taking care to provide meticulous foot care. Wearing boat shoes (specially designed shoes for water wear available in many local stores) can help prevent scraping the feet along the sides or bottom of the pool. Care must be taken to gently dry the feet, especially between the toes, after swimming to prevent infection. Anyone with abrasions or open sores should not enter a swimming pool environment.

A rise in ambient (surrounding) temperature such as a client might experience in an indoor, warm, and humid pool setting also causes an increase in insulin absorption from subcutaneous injection sites. The insulin disappearance rate may be as much as 50% to 60% greater with an increase of 15° in ambient temperature.¹³¹

Additionally, the ease of movement in the water allows increased activity without the same perceived intensity of exertion for the same amount of work performed outside the water. The combination of increased temperatures and increased activity can result in hypoglycemia. The therapist and client must work closely together to maintain a balance of activity, food intake, and insulin dosage.

When a client with diabetes begins aquatic physical therapy, both the time in the water and the intensity of exercise should be systematically progressed and monitored, with one of the parameters being increased with each session according to the client’s tolerance. Before pool therapy, the client must not miss any meals or snacks and must measure blood glucose levels.

A snack or beverage, such as orange juice, should be readily available throughout the therapy session for anyone developing symptoms of hypoglycemia. Glucose testing should be performed after completion of the pool program. Exercise can have a positive effect in reducing blood glucose levels in persons with type 2 DM, but sudden drops in blood glucose levels after exercise should be avoided.

With careful management, the individual should be able to adjust food intake and exercise tolerance to avoid having to increase insulin dosage. Throughout the pool program, the therapist must closely monitor each individual with diabetes for any signs of hypoglycemia (see Table 11-16). The affected individuals must be cautioned to carry out self-monitoring and to respond to the earliest perceived symptoms.

^*Diabetes Self-Management magazine is an invaluable asset for anyone with diabetes. Available by title at PO Box 52890, Boulder, CO 80322-2890 (1-800-234-0923); http://www.diabetesselfmanagement.com

Insulin Resistance Syndrome

Insulin resistance refers to the phenomenon of having high levels of both circulating insulin and glucose in the bloodstream, but the insulin molecules cannot bind properly to the insulin receptor sites on the surface of the cell to allow glucose to enter the cells and be used for energy. A syndrome of insulin resistance has been proposed to explain the frequent association of hypertension, carbohydrate intolerance, abdominal obesity, dyslipidemia, and accelerated atherosclerosis associated with type 2 DM.

Although a primary insufficiency of insulin secretion is the pathology in the development of type 2 DM, obesity is a major risk factor for the development of this type of DM, caused in part by the associated insulin resistance. In 1988 the combination of hypertension, glucose intolerance, hyperinsulinemia, and dyslipidemia was called syndrome X by Gerald Reaven, MD, a diabetes expert, who predicted an increased incidence of coronary heart disease.²⁰²

In the following years, syndrome X was redefined as a prediabetic state and called metabolic syndrome. Criteria for metabolic syndrome include abdominal obesity; elevated triglyceride levels, and low HDLs, hypertension, insulin resistance (with or without glucose intolerance), and proinflammatory markers such as increased C-reactive protein levels or coagulation factors (see Box 12-2).

Even this definition has been through numerous iterations and is still hotly debated. The National Cholesterol Education Program, the World Health Organization, and the American Heart Association all have slightly different versions of the criteria for metabolic syndrome. In contrast, the American Diabetes Association and the European Association for the Study of Diabetes published position statements concluding that there is no disorder called metabolic syndrome. They state that, “there is no solid evidence that any of the metabolic syndrome health factors contribute more together than they do individually. In other words, the whole is not greater than the sum of its parts.”¹¹⁷ The issue is still under debate; see Chapter 12 for further discussion of metabolic disorder.

Obesity and insulin resistance are the underlying factors responsible for the diagnosis of metabolic syndrome. Several definitions of metabolic syndrome have been proposed, but all include insulin resistance or glucose intolerance, hypertension, dyslipidemia, and central obesity. For this reason, the term insulin resistance syndrome (IRS) was suggested by the American College of Endocrinology and the American Association of Clinical Endocrinologists to more aptly describe the prediabetic state.⁶⁴ While IRS has many of the same characteristics of metabolic syndrome, diagnosis is based on a fasting glucose level (100 mg/dl < IRS < 126 mg/dl).

Insulin resistance, a generalized metabolic disorder in which the body cannot use insulin efficiently, appears to play a key role in metabolic syndrome. Although not everyone with insulin resistance has metabolic syndrome, most people with metabolic syndrome are also resistant to the action of insulin.

Regardless of the definition or criteria, most agree that obesity is the single modifiable factor that sets off the cascade. The syndrome is associated with alterations in the abdominal fat cells. With increased fat storage, these cells become distorted in shape, and the receptor site for insulin becomes “warped” or out of proper alignment, so the insulin molecule “key” no longer fits in the receptor. Insulin resistance makes it more difficult to lose weight because the cells are not getting enough fuel and the individual perceives hunger when adequate amounts of circulating glucose exist.

The affected individual may develop elevated blood pressure and problems with reactive hypoglycemia. When the excess insulin is suddenly used, glucose rushes into the cells and the blood glucose drops suddenly. This sequence creates intense sweet cravings, and the cycle repeats itself with increasing insulin resistance.²⁵⁷

The most important implications of recent research indicate that a diagnosis with a syndrome is not necessary in order to treat the individual risk factors. At this prediabetic stage, changes in lifestyle will have the greatest impact on halting any disease progression. In fact, it may be the only time in the disease progression where changes in daily activity levels and nutritional status may have an impact.

11-17 SPECIAL IMPLICATIONS FOR THE THERAPIST

Insulin Resistance Syndrome/Metabolic Syndrome

Physical therapists have a unique opportunity to address IRS/metabolic syndrome through reasonable dietary advice and carefully prescribed exercise counseling. After assessment, physical therapists should guide individuals toward an activity program that includes near-daily exercise that is progressive to a weekly expenditure exceeding 1200 kilocalories of aerobic activity.¹¹⁰

The therapist can provide education regarding the importance of weight loss, exercise, and dietary changes needed to help control dyslipidemia and hypertension. With appropriate lifestyle changes, people can reduce their risk of CVD, prediabetic states, and diabetes.

Studies have not yet determined the ideal exercise program for IRS/metabolic syndrome. Moderate aerobic exercise three times/week based on the ACSM guidelines increases insulin activity in nonobese, nondiabetic subjects despite the fact that there were no changes in weight, BMI, waist-to-hip ratio, lipid profile, or oxygen consumption after 2 months of exercise.⁹⁹

The mechanisms responsible for the improvement in insulin sensitivity after exercise training have been studied extensively but are not fully understood. Research focusing on insulin resistance in skeletal muscle and in particular its relation to changes in aerobic fitness in type 2 diabetes is ongoing.^182,215

Hyperglycemia

Two primary life-threatening metabolic conditions, DKA and hyperosmolar hyperglycemic state (HHS), can develop if uncontrolled or untreated DM progresses to a state of severe hyperglycemia (greater than 300 mg/dl).¹²⁴ Between DKA and HHS is a continuum of metabolic abnormalities.

Diabetic Ketoacidosis:

Definition and Overview.: DKA is most commonly seen in type 1 diabetes when complications develop from severe insulin deficiency. About one-half of the people who require hospitalization for DKA develop this hyperglycemic emergency secondary to an acute infection or failure to follow their prescribed dietary or insulin therapy.²⁵⁹

Most episodes of DKA occur in persons with previously diagnosed type 1 DM. However, the condition may occur in new cases of type 1 and in persons with type 2 DM (under stressful conditions in the latter such as during a myocardial infarction). It is characterized by the triad of hyperglycemia, acidosis, and ketosis.²³⁰

Etiologic Factors.: Any condition that increases the insulin deficit in a person with diabetes can precipitate DKA. Causes of DKA commonly include taking too little insulin; omitting doses of insulin; failing to meet an increased need for insulin because of surgery, trauma, pregnancy, stress, puberty, or infection; and development of insulin resistance caused by insulin antibodies. Other precipitating causes are listed in Box 11-8.

Box 11-8 PRECIPITATING CAUSES OF DIABETIC KETOACIDOSIS^*

• Inadequate insulin under stressful conditions

• Infection

• Missed insulin doses

• Trauma

• Medications

• β-blockers

• Calcium channel blockers

• Pentamidine (NebuPent, Pentam)

• Steroids

• Thiazides (diuretics)

• Alcohol abuse (inability to manage insulin because of mentation change; alcoholic ketoacidosis)

• Hypokalemia

• Myocardial ischemia

• Surgery

• Pregnancy

• Pancreatitis

• Renal failure

• Stroke

^*Listed in descending order.

The most common precipitating factor is infection, which occurs in up to half of all cases and may seem like a trivial condition such as mild cellulitis or upper respiratory tract infection. Omission of insulin, either because of noncompliance or because people mistakenly believe that insulin is not required on sick days when they are not eating well, is another important and preventable cause of DKA.

In young individuals with type 1 DM, psychologic problems complicated by eating disorders may be a contributing factor in 20% of recurrent ketoacidosis. Factors that may lead to insulin omission in younger people include fear of weight gain with improved metabolic control, fear of hypoglycemia, rebellion from authority, and stress of chronic disease. In approximately 15% to 30% of cases, no identifiable cause of DKA can be determined.²³⁰

Pathogenesis.: The initiating metabolic defect in DKA is an insufficient or absent level of circulating insulin. Insulin may be present, but not in a sufficient amount for the increase in glucose resulting from the stressor (see Box 11-8). Inadequate insulin creates a biologic state of starvation, which triggers the excess secretion of counterregulatory hormones, particularly glucagon, in an attempt to get more glucose to the cells and tissues. The abnormal insulin-to-glucagon ratio, with excess circulating cate- cholamine, cortisol, and GH levels, initiates a host of complex metabolic reactions, leading to hyperglycemia, acidosis, and ketosis.

When the body lacks insulin and cannot use carbohydrates for energy, it resorts to fats and proteins. The process of catabolizing fats for fuel gives rise to incomplete lipid metabolism, dehydration, metabolic acidosis, and electrolyte and acid-base imbalances. (See more complete discussion in the section on Pathogenesis of Diabetes Mellitus in this chapter.)

Clinical Manifestations.: The signs and symptoms of DKA vary, ranging from mild nausea to frank coma (Table 11-20). Common symptoms are thirst, polyuria, nausea, and weakness that have progressed over several days. This condition also may develop quickly, with symptoms progressing to coma over the course of only a few hours. Other symptoms may include dry mouth; hot, dry skin; fruity (acetone) odor to the breath, indicating the presence of ketones; overall weakness, possible paralysis; confusion, lethargy, or coma; and deep, rapid respirations (Kussmaul’s respirations). Fever is seldom present even though infection is common, primarily a result of peripheral vasodilation. Severe abdominal pain, possibly accompanied by nausea and vomiting, easily mimics an acute abdominal disorder.

Table 11-20

Clinical Symptoms of Life-Threatening Glycemic States

^*Less gradual than HHS.

Modified from Goodman CC, Snyder TE: Differential diagnosis for physical therapists, ed 4, Philadelphia, 2007, WB Saunders.

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MEDICAL MANAGEMENT

SCREENING.

DIAGNOSIS.

GLUCOSE MONITORING.

TREATMENT.

PROGNOSIS.

Insulin Resistance Syndrome

Hyperglycemia

MEDICAL MANAGEMENT

METABOLIC SYSTEM

Fluid and Electrolyte Balance

Acid-Base Balance

Aging and the Metabolic System

Signs and Symptoms of Metabolic Disease

SPECIFIC METABOLIC DISORDERS

Metabolic Bone Disease

Metabolic Neuronal Diseases

Phenylketonuria

Wilson’s Disease

Porphyrias

References