This is an excerpt from Practical Pharmacology in Rehabilitation With Web Resource by Lynette Carl,Joseph Gallo & Peter Johnson.
Diabetes mellitus is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin, which is a peptide hormone. Insulin is essential in the regulation of carbohydrate fat and protein metabolism in the body. Insulin decreases levels of blood glucose by facilitating the entry of glucose into muscle cells and stimulating the conversion of glucose to glycogen as a storage unit of carbohydrate by a process called glycogenesis. Insulin also inhibits the release of stored glucose from the liver glycogen (glycogenolysis) and slows the breakdown of protein and fat for glucose production (gluconeogenesis) in both the liver and kidneys. Glucose is the sole energy source for red blood cells, the kidneys, and provides energy for the metabolic processes of the brain and central nervous system. Insulin is produced by the beta cells of the islets of Langerhans, located in the pancreas. Maintenance of blood glucose requires a balance between the actions of insulin and glucagon. Incretin hormones, which are released in response to food ingestion, help stimulate insulin secretion and inhibit glucagon secretion.
Globally, 1 in 10 adults has diabetes (World Health Organization, 2012). Diabetes mellitus is expected to affect 380 million people worldwide by 2025. In the United States alone, 24 million adults, or 7% of the population, are diabetics. Diabetes is the leading cause of blindness in adults under 75 yr of age, the leading cause of non-traumatic amputation of the lower extremity (60% of all amputations), and the leading cause of end-stage renal disease. In 2006, diabetes was the seventh leading cause of death (Marquess, 2010; Sherman, 2010).
Etiology and Pathophysiology
Type 1 (insulin-dependent) diabetes occurs when the islets of Langerhans are destroyed and can no longer make insulin. Type 1 diabetes usually develops in childhood and occurs 50% more often in Caucasian Americans than in African Americans or Hispanics. Type 1 diabetes is characterized by uncontrolled hyperglycemia due to the absence of insulin and the associated symptoms which can be fatal if left untreated by insulin replacement. The most easily recognized symptoms of type 1 diabetes are associated with hyperglycemia, Hyperglycemia, defined as fasting blood glucose levels greater than 200 mg/dl, occurs when insulin deficiency allows production of uninhibited amounts of glucose and prevents the use and storage of this circulating glucose. Symptoms associated with hyperglycemia include general malaise, irritability, headache, and weakness. Hyperglycemia can lead to polydipsia (increased thirst) and polyuria (increased frequency and volume of urine). Because the kidneys cannot reabsorb the excess glucose load, glucose spills into the urine (glucosuria), resulting in osmotic diuresis. Osmotic diuresis results in thirst, dehydration, and severe electrolyte imbalance because the water loss is accompanied by loss of electrolytes. Inability of tissues to use glucose causes breakdown of fat and protein to meet energy needs, leading to ketone production and weight loss. Failure to thrive and wasting may be the first symptom of diabetes in the infant or child (Lamb, 2011; Marquess, 2010; Sherman, 2010).
Many diabetics are initially diagnosed with diabetes after presenting to the emergency room with diabetic ketoacidosis. Diabetic ketoacidosis is a life-threatening syndrome of extremely high glucose levels, severe dehydration, and electrolyte imbalance. It is accompanied by ketones in the blood, respiratory distress, hypotension, tachycardia, vomiting, and altered mental status that may present as diabetic coma. Treatment requires hospitalization, replacement of fluids and electrolytes, and administration of an insulin drip to stabilize the patient (Marquess, 2010; Sherman, 2010).
Type 2 diabetes (non-insulin-dependent) is characterized by peripheral insulin resistance and an insulin secretory defect (as opposed to insulin deficiency in type 1 diabetes). Most diabetics (90%-95%) are type 2 diabetics, and most are obese. All overweight persons have insulin resistance, but diabetes develops in those who are not able to increase beta-cell production to compensate for the insulin resistance. Weight loss can normalize blood glucose in these patients. More children are being diagnosed with type 2 diabetes, and most of those diagnosed have associated childhood obesity.
When working with the diabetic patient, the rehabilitation therapist should check whether the patient's medications have changed since the last therapy session and should consider the scheduling of medications and meals when designing sessions. Many patients with diabetes require a snack before exercise to prevent hypoglycemia. Hypoglycemia, which can occur in both type 1 and type 2 diabetics, is characterized by nausea, extreme hunger, jitteriness, cold or clammy skin, excessive perspiration, tachycardia, numbness of fingertips or lips, and trembling. If blood glucose falls below 55 mg/dl, altered mental status, along with irritability, anxiety, restlessness, confusion, and difficulty thinking or concentrating can occur. Difficulty in ambulation, blurred vision, lethargy, and slurred speech can also occur. If blood glucose decreases below 40 mg/dl, seizures, loss of consciousness, and coma can occur (Marquess, 2010; Sherman, 2010).
The therapist should monitor the patient for symptoms of hyperglycemia or hypoglycemia during the session and make appropriate interventions to reduce fall risk associated with fluctuations in glucose levels in the diabetic patient. The therapist should ensure that the patient receives education regarding appropriate diet, exercise, smoking cessation, and foot care. The patient should be assisted by a clinical dietitian in developing an appropriate diet plan and should receive education about how diet and exercise affects the control of glucose and cholesterol levels. The clinical pharmacist can provide additional education about the appropriate use of blood glucose monitoring and use of medications to control diabetes, hypertension, and high cholesterol in order to reduce risk of diabetic complications (DeHart & Worthington, 2005).
In addition to diet and medication therapy, other forms of therapy in diabetic neuropathy are useful. Physical therapy may be a useful when the patient's neuropathy manifests in muscle pain and weakness. The physical therapist can instruct the patient in general exercise techniques for maintaining mobility and strength and in pain-management and relaxation strategies. The physical therapist can also provide transcutaneous electrical nerve stimulation treatment for neuropathic pain and assist with wound care of diabetic foot ulcers using modalities of whirlpool treatment and debridement. Patients with autonomic neuropathy need balance training and fall-prevention education. The therapist also determines whether the patient requires braces, orthotics, prosthetics, or assistive devices to promote safe and efficient gait and functional performance (Brock, 2010; Montfort et al., 2010; Sherman, 2010; Votey & Peters, 2010; White, 2010).
Patients with severe loss of function may need occupational therapy. When only the lower limbs are involved, patients may need home modifications and equipment. When the upper limbs are involved, patients may need more extensive functional restoration and adaptive equipment. When a person loses a limb, even more intensive functional retraining is required. Involvement of a speech-language pathologist can help patients affected by gastroparesis or dysphagia (Brock, 2010; Montfort et al., 2010; Sherman, 2010; Votey & Peters, 2010; White, 2010).
Surgical intervention is indicated in the case of aggressive debridement or an amputation for necrosis or infection of a diabetic foot ulcer, insertion of a jejunostomy tube in order to feed the patient with intractable gastroparesis by bypassing the paralytic stomach, or penile prosthesis for impotence not responsive to alternative therapy. Treatment of Charcot joint (denervated joint deformity associated with osteoporosis) may include surgery to correct the deformity along with bracing and placing the joint in a boot (Brock, 2010; Montfort et al., 2010; Sherman, 2010; Votey & Peters, 2010; White, 2010).
Patient Case 1
J.K. is a 23-yr-old female college volleyball player with a history of diabetes who was referred to her athletic trainer for help developing a regimen of strength-training exercises. She is 5 ft 8 in. (1.72 m) tall and weighs 125 lb (56.7 kg). She reports difficulty finishing a game due to weakness, extreme thirst, and headaches despite carbohydrate loading and drinking sport drinks before the game.
What actions should the athletic trainer take at this time?
J.K. is exhibiting symptoms of hyperglycemia, probably due to consumption of inappropriate carbohydrate drinks before the game. The patient is most likely a type 1 (insulin-dependent) diabetic. J.K.'s blood glucose should be checked and insulin should be administered as prescribed by her physician. J.K. should be instructed to have a snack of complex carbohydrates rather than a high-sugar drink before exercise. The athletic trainer should ask about J.K.'s medications, her diet regimen, and how often she monitors her glucose levels and provide follow-up education and referral as needed.
Long-term complications associated with type 1 and type 2 diabetes include increased risk of infections; microvascular complications of retinopathy, cataracts, nephropathy, or progressive renal failure; neuropathic complications; and macrovascular disease leading to coronary artery disease, hypertension, myocardial infarction, or stroke. Macrovascular complications such as stroke or myocardial infarction is the leading cause of death in patients with diabetes. They cause up to 75% of deaths in diabetics compared with 35% of deaths in patients without diabetes. Diabetes increases the risk of myocardial infarction twofold in men and fourfold in women. Because atherosclerosis occurs earlier in the diabetic and is more severe in patients with this disease, aggressive treatment of dyslipidemia with medications such as statins is required to avoid these complications in patients with diabetes. The risk of hypertension in the diabetic is twice that in the nondiabetic. Medications that reduce hypertension to control glucose levels should be initiated early and used to aggressively control blood pressure and blood glucose in order to reduce complications associated with macrovascular disease. An angiotensin-converting enzyme inhibitor should be used in the diabetic patient to reduce blood pressure and protect against diabetic nephropathy.
Infections can cause considerable morbidity and mortality in the diabetic. Diabetics can have poor tissue perfusion, decreased sensation due to peripheral neuropathy, and impaired immunity that increases the risk of developing infections. Neuropathy associated with diabetes includes peripheral and autonomic neuropathy, and a symmetric distal sensori-motor neuropathy in a stocking-and-glove distribution is commonly seen. Loss of peripheral sensation allows foot injury to go undetected and can result in diabetic foot ulcers (Sherman, 2010).
Prolonged hyperglycemia causes several biological changes, including an increase in the attachment of glucose to tissues producing glycosylated products. Glycosylated hemoglobin (hemoglobin A1C) is used as a laboratory marker for tracking long-term glycemic control over a period of several months. For every point decrease in hemoglobin A1C, patients can reduce their risk of microvascular complications by 40%. The American Diabetes Association recommends a target hemoglobin A1C level of 7%, the American Association of Clinical Endocrinologists recommends a hemoglobin A1C level of 6.5% or lower. The Diabetes Control and Complications Trial, which studied outcomes in patients with type 1 diabetes, and the United Kingdom Prospective Diabetes Study, which studied outcomes in patients with type 2 diabetes, both showed that lowering glucose levels and associated hemoglobin A1C levels resulted in lowered risk for microvascular and macrovascular disease (Marquess, 2010; Sherman, 2010).
Patient Case 1, continued
When speaking with J.K., the athletic trainer learns that J.K. has had diabetes since she was 8 yr old. J.K. takes long-acting insulin each morning and checks her blood sugar every morning before taking her insulin. Her physician has asked her to check her blood sugar more often, but she finds it inconvenient.
What can the athletic trainer tell J.K. about the importance of checking her blood sugar more often and maintaining normal glucose throughout the day?
The athletic trainer should tell J.K. that checking blood glucose levels more frequently (usually before each meal and at bedtime) and maintaining normal blood glucose levels throughout the day (hemoglobin A1C level
Patient Case 1, continued
At her next rehabilitation session, J.K. mentions that she does not feel well when she exercises. She wonders whether she is better off not exercising at all.
How should the athletic trainer advise J.K.?
The athletic trainer should explain that exercise is an important aspect of managing diabetes and that patients should exercise regularly with an exercise plan approved by their physician. Exercise can improve blood pressure and cholesterol levels and help maintain normal glucose levels (euglycemia). The therapist should advise J.K. that exercising vigorously for more than 30 min lowers glucose levels and can cause symptoms of hypoglycemia. To prevent hypoglycemia, the physician may advise J.K. to decrease her insulin by 10% to 20% or consume an extra snack before exercise. The therapist should also stress the importance of maintaining hydration status during exercise with water rather than sport drinks that contain caffeine and sugar (Sherman, 2010).
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