Diabetes mellitus with complication

All about Diabetes Mellitus and its complications

1. Diabetes Mellitus Mrs Dipali Dumbre Msc Nursing Medical Surgical Nursing SCON

2. Definition Diabetes mellitus is a chronic multisystem disease related to abnormal insulin production, impaired insulin utilization, or both.

3. Etiology Heredity Autoimmune Viral environmental factors (e.g., stress). Regardless of its cause, diabetes is primarily a disorder of glucose metabolism related to absent or insufficient insulin supplies and/or poor utilization of the insulin that is available.

4. Classification The two most common types of diabetes are classified as Type 1 diabetes mellitus Type 2 diabetes mellitus Other classifications of diabetes commonly seen in clinical practice Gestational diabetes Prediabetes secondary diabetes

5. Type 1 diabetes mellitus Formerly known as “juvenile onset” or “insulin-dependent” diabetes. Type 1 diabetes mellitus most often occurs in people who are under 30 years of age, with a peak onset between ages 11 and 13, but it can occur at any age. Typically, it is seen in people with a lean body type, although it can occur in people who are overweight. Type 1 diabetes mellitus

6. Etiology Type 1 diabetes is the end result of a long-standing process in which the body's own T cells attack and destroy pancreatic beta (β) cells, which are the source of the body's insulin. Autoantibodies to the islet cells cause a reduction of 80% to 90% of normal β-cell function before hyperglycemia . A genetic predisposition and exposure to a virus are factors that may contribute to the pathogenesis of immune-related type 1 diabetes.

7. Type 1 diabetes may be caused by nonimmune factors of unknown (idiopathic) etiologies is known as type 1B diabetes. When type 1 diabetes is caused by an immune mechanism, the disease is known as type 1A.

8. Onset of Disease Type 1 diabetes is associated with a long preclinical period. The islet cell autoantibodies responsible for β-cell destruction are present for months to years before the onset of symptoms. Manifestations of type 1 diabetes develop when the person's pancreas can no longer produce insulin. The onset of symptoms is usually rapid, and the patient comes to the emergency department with impending or acute ketoacidosis.

9. The patient usually has a history of recent and sudden weight loss. The classic symptoms of Polydipsia (excessive thirst) Polyuria (frequent urination) Polyphagia (excessive hunger) The individual with type 1 diabetes requires a supply of insulin from an outside source (exogenous insulin), such as an injection, in order to sustain life. Without insulin, the patient will develop diabetic ketoacidosis (DKA), a life-threatening condition resulting in metabolic acidosis.

10. Newly diagnosed patients with type 1 diabetes often experience a remission, or “honeymoon period,” soon after treatment is initiated. During this time, the patient requires very little injected insulin because β-cell mass remains sufficient for glucose control as the progressive destruction continues to occur. Eventually, as more β cells are destroyed, blood glucose levels increase, more insulin is needed, and the honeymoon period ends. The honeymoon period usually lasts 3 to 12 months, after which the person will require insulin on a permanent basis.

11. Prediabetes Prediabetes, also known as impaired glucose tolerance (IGT) or impaired fasting glucose, is a condition in which blood glucose levels are higher than normal (>100 mg/dl but <126 mg/dl [7.0 mmol /L] when fasting) but not high enough for a diagnosis of diabetes . Most people with prediabetes are at increased risk for developing type 2 diabetes, and if no preventive measures are taken, they will usually develop it within 10 years. Long-term damage to the body, especially the heart and blood vessels, may already be occurring in patients with prediabetes .

12. People with prediabetes usually do not have symptoms. Individuals with prediabetes should test their blood glucose regularly and watch for the symptoms of diabetes, such as polyuria , polyphagia , or polydipsia . If action is taken to manage blood glucose, patients with prediabetes can delay or prevent the development of type 2 diabetes. Maintaining a healthy weight, exercising regularly, and eating a healthy diet have all been found to reduce the risk of developing diabetes in people with prediabetes .

13. Gestational Diabetes Gestational diabetes develops during pregnancy . It is detected at 24 to 28 weeks of gestation. Women with gestational diabetes have a higher risk for cesarean delivery, perinatal death, and neonatal complications. Although most women with gestational diabetes will have normal glucose levels within 6 weeks postpartum, Their risk for developing type 2 diabetes in 5 to 10 years is increased. Nutritional therapy is considered to be the first-line therapy. If nutritional therapy alone does not achieve desirable fasting blood glucose levels, insulin therapy is usually indicated.

14. Secondary Diabetes Diabetes occurs because of another medical condition or due to the treatment of a medical condition that causes abnormal blood glucose levels. Conditions that may cause secondary diabetes can result from damage to, injury to, interference with, or destruction of the pancreas.

15. These include Cushing syndrome, hyperthyroidism, recurrent pancreatitis, and the use of parenteral nutrition. Commonly used medications that can induce diabetes include corticosteroids (prednisone), thiazides , phenytoin , and atypical antipsychotics . Secondary diabetes usually resolves when the underlying condition is treated.

16. Type 2 Diabetes Mellitus Definition : “The pancreas usually continues to produce some endogenous (self-made) insulin, the insulin that is produced is either insufficient for the needs of the body and/or is poorly utilized by the tissues.”

17. Type 2 diabetes mellitus is, by far, the most prevalent type of diabetes, accounting for over 90% of patients with diabetes. Type 2 diabetes usually occurs in people over 35 years of age, and 80% to 90% of patients are overweight at the time of diagnosis.

18. Etiology In type 2 diabetes the insulin that is produced is either insufficient for the needs of the body and/or is poorly utilized by the tissues. Risk factor are: Obesity, specifically abdominal and visceral adiposity. Metabolic syndrome is a cluster of abnormalities that act synergistically to greatly increase the risk for cardiovascular disease and diabetes.

19. Metabolic syndrome is characterized by Insulin resistance Elevated insulin levels High levels of triglycerides (more than 150mg/dl) Decreased levels of high-density lipoproteins (HDLs) Increased levels of low-density lipoproteins (LDLs) Hypertension

20. Pathophysiology First Factor is Insulin resistance: Insulin resistance in glucose and lipid metabolism, which is a condition in which body tissues do not respond to the action of insulin. This is due to insulin receptors that are either unresponsive to the action of insulin and/or insufficient in number. Most insulin receptors are located on skeletal muscle, fat, and liver cells. When insulin is not properly used, the entry of glucose into the cell is impeded, resulting in hyperglycemia.

21. A second factor in the development of type 2 diabetes is a marked decrease in the ability of the pancreas to produce insulin, as the β cells become fatigued from the compensatory overproduction of insulin or when β-cell mass is lost. A third factor is inappropriate glucose production by the liver. Instead of properly regulating the release of glucose in response to blood levels, the liver does so in a haphazard way that does not correspond to the body's needs at the time.

22. A fourth factor is alteration in the production of hormones and cytokines by adipose tissue ( adipokines ). Adipokines appear to play a role in glucose and fat metabolism.

23. Onset of Disease Disease onset in type 2 diabetes is usually gradual. The person may go for many years with undetected hyperglycemia that might produce few symptoms. If the patient with type 2 diabetes has marked hyperglycemia a sufficient endogenous insulin supply may prevent DKA from occurring. However, osmotic fluid and electrolyte loss related to hyperglycemia may become severe and lead to hyperosmolar coma.

24. Clinical Manifestation The clinical manifestations of type 2 diabetes are often nonspecific. Fatigue Recurrent infections Prolonged wound healing Blurred vision Weight loss

25. Diagnostic studies Fasting plasma glucose level ≥126 mg/dl. Fasting is defined as no caloric intake for at least 8 hours. Random glucose measurement ≥200 mg/dl) Two-hour OGTT level ≥200 mg/dl (11.1 mmol /L), using a glucose load of 75 g. When overt symptoms of hyperglycemia ( polyuria , polydipsia , and polyphagia ) coexist with FPG levels of 126 mg/dl or greater, further testing using the OGTT may not be necessary to make a diagnosis

26. Measurement of glycosylated hemoglobin, also known as the hemoglobin A1C (A1C) test . A1C tests are used by diabetic patients and health care providers to monitor success of treatment and to make changes in treatment modalities. It is not used as a diabetes diagnostic test. The test works by showing the amount of glucose that has been attached to hemoglobin molecules over their life span.

27. When blood glucose is elevated over time, the amount of glucose attached to the hemoglobin molecule increases and remains attached to the red blood cell (RBC) for the life of the cell (approximately 120 days). Therefore a glycosylated hemoglobin test indicates the overall glucose control for the previous 90 to 120 days. All patients with diabetes should have regular assessments of A1C done. For people with diabetes, the ideal A1C goal is 7.0% or less

28. Procedure for OGTT A zero time (baseline) blood sample is drawn. The patients is then given 75g of glucose solution to drink within a 5 minute time frame. The blood is drawn as per the interval but usually 2 hours interval is taken.

29. Collaborative care The goals of diabetes management are to reduce symptoms, promote well-being, prevent acute complications of hyperglycemia,. These goals are most likely to be met when the patient is able to maintain blood glucose levels as near to normal as possible. Diabetes is a chronic disease that requires daily decisions about food intake, blood glucose testing, medication, and exercise.

30. Patient teaching, which enables the patient to become the most active participant in his or her own care, is essential for a successful treatment plan. Nutritional therapy, drug therapy, exercise, and self-monitoring of blood glucose are the tools used in the management of diabetes .

31. Drug Therapy Exogenous (injected) insulin is needed when a patient has inadequate insulin to meet specific metabolic needs. People with type 1 diabetes require exogenous insulin to survive and may need up to four to five injections per day to adequately control blood glucose levels. People with type 2 diabetes, who are usually controlled with diet, exercise, may require exogenous insulin temporarily during periods of severe stress such as illness or surgery.

32. Types of Insulin In the past, insulin was made from beef and pork pancreas, but these forms of insulin are no longer available. Today, only human insulin is used. Human insulin is not directly harvested from human organs. Instead, it is prepared through the use of genetic engineering. The insulin is derived from common bacteria (e.g., Escherichia coli ) or yeast cells using recombinant DNA technology .

33. Insulin differ in regard to onset, peak action, and duration and are categorized as Rapid-acting, Short-acting, Intermediate-acting Long-acting insulin. The specific properties of each type of insulin are matched with the patient's diet and activity. Various combinations of these insulin can be used to give treatment to the patient's specific pattern of blood glucose levels, lifestyle, eating, and activity patterns.

34. Insulin preparations showing onset, peak, and duration of action

35. Types of Insulin CLASSIFICATION EXAMPLES: CLARITY OF SOLUTION Rapid-acting insulin Lispro ( Humalog ), clear Aspart ( NovoLog ), clear Glulisine ( Apidra ), clear Short-acting insulin Regular ( Humulin R, Novolin R, ReliOn R), clear Intermediate-acting insulin NPH ( Humulin N, Novolin N, ReliOn N), cloudy Long-acting insulin Glargine ( Lantus ), clear Detemir ( Levemir ), clear Combination therapy (premixed) NPH/regular 70/30 ( Humulin 70/30, Novolin 70/30, ReliOn 70/30), cloudy NPH/regular 50/50 * ( Humulin 50/50), cloudy

36. Rapid acting insulin analog have an onset of action of approximately 15 minute and should be injected 0 to 15 min before the meal. Short acting regular insulin has an onset of action 30 to 60 mintues and should be injected 30 to 45minute before a meal to ensure that the onset of action coincides with meal absorption. Long –acting insulins are released steadily and continuously, they are used for once-daily . Short or rapid-acting insulin is often mixed with intermediate –acting insulin to provide both mealtime and basal coverage without having to administer two separate injections

37. Insulin Regimens. The timing of insulin administration in relation to meal is very important. Regular insulin is taken 30 to 45 minutes before meals to ensure the onset of action in conjunction with meal absorbtion . Ideally, regimens should be mutually selected by the patient and the health care provider. The criteria for selection are based on the desired and feasible levels of glycemic control and the patient's lifestyle.

38. Storage of insulin As a protein, insulin requires special storage considerations. Heat and freezing alter the insulin molecule. Insulin vials that the patient is currently using may be left at room temperature for up to 4 weeks unless the room temperature is higher than 86° F (30° C) or below freezing (less than 37° F [2° C]). Prolonged exposure to direct sunlight should be avoided. Extra insulin should be stored in the refrigerator. Prefilled syringes are stable for up to 30 days when stored in the refrigerator. Syringes prefilled with a cloudy solution should be stored in a vertical position with the needle pointed up to avoid clumping of suspended insulin binders in the needle.

39. Administration of Insulin

40. Injection sites for insulin

41. Problems with Insulin Therapy Allergic Reactions. Local inflammatory reactions to insulin may occur, such as itching, erythema , and burning around the injection site. Local reactions may be self-limiting within 1 to 3 months or may improve with a low dose of antihistamine. Lipodystrophy . Lipodystrophy (atrophy of subcutaneous tissue) may occur if the same injection sites are used frequently. It is best prevented by rotation of injection sites. Hypertrophy, a thickening of the subcutaneous tissue, eventually regresses if the patient does not use the site for at least 6 months. The use of hypertrophied sites may result in erratic insulin absorption.

42. Somogyi Effect and Dawn Phenomenon. The Somogyi effect is a rebound effect in which an overdose of insulin induces hypoglycemia. Usually occurring during the hours of sleep, the Somogyi effect produces a decline in blood glucose level in response to too much insulin. Counterregulatory hormones are released, stimulating lipolysis , gluconeogenesis , and glycogenolysis , which in turn produce rebound hyperglycemia . The danger of this effect is that when blood glucose levels are measured in the morning, hyperglycemia is apparent and the patient (or the health care professional) may increase the insulin dose. The patient may report headaches on awakening and may recall night sweats or nightmares.

43. If the Somogyi effect is suspected as a cause for early morning high blood glucose, the patient may be advised to check blood glucose levels between 2:00 and 4:00 am to determine if hypoglycemia is present at that time. If it is, the insulin dosage affecting the early morning blood glucose is reduced. Dawn phenomenon : It is characterized by hyperglycemia that is present on awakening in the morning due to the release of counterregulatory hormones in the predawn hours. It has been suggested that growth hormone and cortisol are possible factors in this occurrence. The dawn phenomenon affects the majority of people with diabetes and tends to be most severe when growth hormone is at its peak in adolescence and young adulthood.

44. Drug Therapy: Oral Agents Oral agents (OAs) are not insulin, but they work to improve the mechanisms by which insulin and glucose are produced and used by the body. OAs work on the three defects of type 2 diabetes: (1) insulin resistance (2) decreased insulin production (3) increased hepatic glucose production. OAs may be used in combination with agents from other classes or with insulin to achieve blood glucose targets.

45. Nutritional Therapy The overall goal of nutritional therapy is to assist people with diabetes in making healthy nutritional choices, eating a varied diet, and maintaining exercise habits that will lead to improved metabolic control. Maintain blood glucose levels to as near normal as safely possible to prevent or reduce the risk for complications of diabetes. Achieve lipid profiles and blood pressure levels that reduce the risk for cardiovascular disease. Modify lifestyle as appropriate for the prevention and treatment of obesity, dyslipidemia , cardiovascular disease, and nephropathy. Improve health through healthy food choices and physical activity. Address individual nutritional needs while taking into account personal and cultural preferences and respecting the individual's willingness to change.

46. Food Composition. Carbohydrates. In the diabetic meal plan, carbohydrates and monounsaturated fats should provide 45% to 65% of the total energy intake each day. Carbohydrates include sugars, starches, and fiber. Foods containing carbohydrates from whole grains, fruits, vegetables, and low-fat milk should be included as part of a healthy meal plan. 21 Glycemic index (GI) is the term used to describe the rise in blood glucose levels after a person has consumed a carbohydrate-containing food. A GI of 100 refers to the response of 50 g of glucose or white bread in a normal person without diabetes. All other food with an equivalent carbohydrate value is measured against this standard. For example, the GI of an apple is 52, regular milk 27, baked potato 93, cornflake cereal 119, and baked beans 69. The GI of carbohydrates should be considered when choosing them in a meal plan. Foods with a high GI (e.g., potatoes, white bread) will cause a sharp rise in blood glucose, whereas those with a low GI (e.g., brown rice), steadily increase blood glucose over a longer period of time.

47. Fats Fat should compose no more than 25% to 30% of the meal plan's total calories, with less than 7% of calories from saturated fats. Less than 300 mg/day of cholesterol and limited trans fats are also recommended as part of a healthy meal plan. Decreasing fat and cholesterol intake assists in reducing the risk for cardiovascular disease. Individuals with elevated LDL are advised to lower their saturated fat intake to 7% and cholesterol to under 200 mg/day.

48. Protein. Protein should contribute less than 10% of the total energy consumed in those with diabetes. Protein intake for the diabetic patient should be significantly lower than the general population. Alcohol. Alcohol is high in calories, has no nutritive value, and promotes hypertriglyceridemia . The inhibitory effect of alcohol on glucose production by the liver can cause severe hypoglycemia in patients on insulin or oral hypoglycemic medications that increase insulin secretion. Patients should be cautioned to honestly discuss the use of alcohol with their health care providers because its use can make blood glucose more difficult to control. Moderate alcohol consumption can sometimes be safely incorporated into the meal plan if blood glucose levels are well controlled and if the patient is not on medications that will cause adverse effects. Moderate consumption is defined as one drink per day for women and two drinks per day for men.

49. Exercise for Patients with Diabetes Mellitus 1. Exercise does not have to be vigorous to be effective. The blood glucose–reducing effects of exercise can be attained with exercise such as brisk walking. 2. The exercises selected should be enjoyable to foster regularity. 3. The exercise session should have a warm-up period and a cool-down period. The exercise program should be started gradually and increased slowly. 4. Exercise is best done after meals, when the blood glucose level is rising. 5. Exercise plans should be individualized for each patient and monitored by the health care provider.

50. 6. It is important to self-monitor blood glucose levels before, during, and after exercise to determine the effect exercise has on blood glucose level at particular times of the day. Before exercise, if blood glucose is less than 100 mg/dl, eat a 10-15 g carbohydrate snack. After 15 to 30 minutes, retest blood glucose levels. Do not exercise if less than 100 mg/dl. Before exercise, if blood glucose is over 250 mg/dl, delay exercise or if patient insists on exercising, reduce the intensity and duration by half. Recheck blood glucose at the end of the exercise program. 7. Be alert to the possibility of delayed exercise-induced hypoglycemia, which may occur several hours after the completion of exercise. 8. Taking a glucose-lowering medication does not mean that planned or spontaneous exercise cannot occur. 9. It is important to compensate for extensive planned and spontaneous activity by monitoring blood glucose level to make adjustments in the insulin dose (if taken) and food intake.

51. Self-Monitoring of Blood Glucose (SMBG) 1. Wash hands in warm water. It is not necessary to clean the site with alcohol, and it may interfere with test results. Finger should be dry before puncturing it. 2. If it is difficult to obtain an adequate drop of blood for testing, warm the hands in warm water or let the arms hang dependently for a few minutes before the finger puncture is made. 3. If the puncture is made on the finger, use the side of the finger pad rather than near the center. Fewer nerve endings are along the side of the finger pad. 4. The puncture should be only deep enough to obtain a sufficiently large drop of blood. Unnecessarily deep punctures may cause pain and bruising. 5. Follow monitor instructions for testing the blood. 6. Record results. Compare to personal target blood glucose goals.

52. Complications of diabetes mellitus

53. Complications of diabetes mellitus Acute complications: Ketoacidosis The hyperglycemic hyperosmolar nonketotic syndrome Hypoglycemia Chronic complications: Disorders of the microcirculation Neuropathies Nephropathies Retinopathies Macrovascular complications Foot ulcers

54. Diabetic Ketoacidosis

55. Definition Diabetic ketoacidosis (DKA), also referred to as diabetic acidosis and diabetic coma, is caused by a profound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, and dehydration.

56. Etiology Type 1 diabetes Type 2 diabetes in conditions of severe illness or stress when the pancreas cannot meet the extra demand for insulin. Precipitating factors include Illness and infection Inadequate insulin dosage Undiagnosed type 1 diabetes Poor self-management, and neglect.

57. Pathophysiology When the circulating supply of insulin is insufficient, glucose cannot be properly used for energy so that the body breaks down fat stores as a secondary source of fuel . Ketones are acidic by-products of fat metabolism that can cause serious problems when they become excessive in the blood. Ketosis alters the pH balance, causing metabolic acidosis .

58. Ketonuria is a process that begins when ketone bodies are excreted in the urine. During this process, electrolytes become depleted as cations are eliminated along with the anionic ketones in an attempt to maintain electrical neutrality. Insulin deficiency impairs protein synthesis and causes excessive protein degradation.

59. Insulin deficiency also stimulates the production of glucose from amino acids in the liver and leads to further hyperglycemia. Because there is a deficiency of insulin, the additional glucose cannot be used and the blood glucose level rises further, adding to the osmotic diuresis . Untreated, this leads to severe depletion of sodium, potassium, chloride, magnesium, and phosphate. Vomiting caused by the acidosis results in more fluid and electrolyte losses.

60. Eventually, hypovolemia followed by shock. Renal failure may eventually occur from hypovolemic shock. This causes the retention of ketones and glucose, and the acidosis progresses. Untreated, the patient becomes comatose as a result of dehydration, electrolyte imbalance, and acidosis. If the condition is not treated, death is inevitable.

61. Clinical Manifestation Dehydration such as poor skin turgor , Dry mucous membranes, Tachycardia, Orthostatic hypotension. Lethargy and weakness. As the patient becomes severely dehydrated, the skin becomes dry and loose, and the eyeballs become soft and sunken. Abdominal pain is another symptom of DKA that may be accompanied by anorexia and vomiting.

62. Finally, Kussmaul respirations (rapid, deep breathing associated with dyspnea ) are the body's attempt to reverse metabolic acidosis through the exhalation of excess carbon dioxide. Acetone is noted on the breath as a sweet, fruity odor. Laboratory findings include a blood glucose level above 300 mg/dl . arterial blood gas pH below 7.30, serum bicarbonate level less than 15 mEq /L (15 mmol /L), Ketones in the blood and urine.

63. Diagnostic Studies History and physical examination Blood studies, including immediate blood glucose, complete blood count, Ketones , pH, electrolytes, Blood urea nitrogen Arterial blood gases Urinalysis, including specific gravity, pH, glucose, acetone

64. EMERGENCY MANAGEMENT: Etiology Undiagnosed diabetes mellitus • Inadequate treatment of existing diabetes mellitus • Insulin not taken as prescribed • Infection • Change in diet, insulin, or exercise regimen Assessment findings • Thirst • Abdominal pain • Nausea and vomiting • Gradually increasing restlessness, confusion, lethargy

65. • Flushed, dry skin • Eyes appear sunken • Breath odor of ketones • Rapid, weak pulse • Labored breathing ( Kussmaul respirations) • Fever • Urinary frequency • Serum glucose 300 mg/dl (16.7 mmol /L) • Glucosuria and ketonuria

66. Collaborative Management Administration of intravenous fluids Intravenous administration of rapid-acting insulin Electrolyte replacement Assessment of mental status Recording of intake and output Central venous pressure monitoring (if indicated) Assessment of blood glucose levels Assessment of blood and urine for ketones ECG monitoring Assessment of cardiovascular and respiratory status ECG, Electrocardiogram.

67. Intervention: Initial • Ensure patent airway. • Administer oxygen. • Establish IV access with large-bore catheter. • Begin fluid resuscitation with 0.9% NaCl solution 1 L/hr until BP stabilized and urine output 30-60 ml/hr. • Begin continuous regular insulin drip 0.1 U/kg/hr. • Identify history of diabetes, time of last food, and time/amount of last insulin injection.

68. Ongoing Monitoring • Monitor vital signs, level of consciousness, cardiac rhythm, oxygen saturation, and urine output. • Assess breath sounds for fluid overload. • Monitor serum glucose and serum potassium. • Administer potassium to correct hypokalemia . • Administer sodium bicarbonate if severe acidosis (pH 7.0).

69. The hyperglycemic hyperosmolar nonketotic (HHNK) syndrome Hyperosmolar hyperglycemic  state (HHS) is a complication of diabetes mellitus (predominantly type 2) in which high blood sugars cause severe dehydration, increases in osmolality In hyperosmolar states, the increased serum osmolality has the effect of pulling water out of body cells, including brain cells. The condition may be complicated by thromboembolic events arising because of the high serum osmolality. The most prominent manifestations are dehydration: Neurologic signs and symptoms: S eizures Hemiparesis Aphasia

70. Muscle fasciculations Hyperthermia Nystagmus Visual hallucinations Excessive thirst The onset of HHNK syndrome often is insidious, and because it occurs most frequently in older people, it may be mistaken for a stroke . The main difference between HHS and DKA is that the patient with HHS usually has enough circulating insulin so that ketoacidosis does not occur.

71. Pathophysiology

72. Treatment HHS constitutes a medical emergency and has a high mortality rate. Therapy is similar to that for the treatment of DKA and includes immediate IV administration of either 0.9% or 0.45% NaCl . Regular insulin is given by IV bolus, followed by an infusion after fluid replacement therapy is instituted to aid in reducing the hyperglycemia . When blood glucose levels fall to approximately 250 mg/dl (13.9 mmol /L), IV fluids containing glucose are administered to prevent hypoglycemia. Electrolytes are monitored and replaced as needed. Vital signs, intake and output, tissue turgor, laboratory values, and cardiac monitoring are assessed to monitor the efficacy of fluid and electrolyte replacement. Patients with renal or cardiac compromise require special monitoring to avoid fluid overload during fluid replacement. This includes monitoring of serum osmolality and frequent assessment of cardiac, renal, and mental status.

73. Hypoglycemia Hypoglycemia occurs from a relative excess of insulin in the blood and is characterized by below-normal blood glucose levels. It occurs most commonly in people treated with insulin injections, but prolonged hypoglycemia also can result from some oral hypoglycemic agents.

74. Many factors precipitate an insulin reaction in a person with type 1 diabetes, including: Error in insulin dose Failure to eat Increased exercise Decreased insulin need after removal of a stress situation Medication changes and a change in insulin site Alcohol decreases liver gluconeogenesis, and people with diabetes need to be cautioned about its potential for causing hypoglycemia.

75. Because the brain relies on blood glucose as its main energy source, hypoglycemia produces behaviors related to altered cerebral function: Headache Difficulty in problem solving Disturbed or altered behavior Coma Seizures At the onset of the hypoglycemic episode, activation of the parasympathetic nervous system often causes hunger. The initial parasympathetic response is followed by activation of the sympathetic nervous system; this causes anxiety, tachycardia, sweating, and constriction of the skin vessels ( i.e. , the skin is cool and clammy).

76. Treatment The most effective treatment of an insulin reaction is the immediate ingestion of a concentrated carbohydrate source, such as sugar, honey, candy, or orange juice. Alternative methods for increasing blood glucose may be required when the person having the reaction is unconscious or unable to swallow: Glucagon may be given intramuscularly or subcutaneously. In situations of severe or life-threatening hypoglycemia, it may be necessary to administer glucose intravenously.

77. Macrovascular complications Macrovascular complications are diseases of the large and medium-size blood vessels that occur with greater frequency and with an earlier onset in people with diabetes. Diabetes mellitus is a major risk factor for coronary artery disease, cerebrovascular disease, and peripheral vascular disease. Multiple risk factors for vascular disease, including obesity, hypertension, hyperglycemia, hyperlipidemia, altered platelet function , are found in people with diabetes. In people with type 2 diabetes, macrovascular disease may be present at the time of diagnosis. In type 1 diabetes, the attained age and the duration of diabetes appear to correlate with the degree of macrovascular disease.

78. MICROVASCULAR COMPLICATIONS “ Microvascular complications result from thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia .’”

79. Peripheral neuropathies Diabetic neuropathy is nerve damage that occurs because of the metabolic derangements associated with diabetes mellitus . About 60% to 70% of patients with diabetes have some degree of neuropathy, with neurologic complications occurring equally in type 1 and type 2 diabetes. The most common type of neuropathy affecting persons with diabetes is sensory neuropathy . This can lead to the loss of protective sensation in the lower extremities and complications that result in a lower limb amputation.

80. Classification The two major categories of diabetic neuropathy are sensory neuropathy, which affects the peripheral nervous system, and autonomic neuropathy . Each of these types can take on several forms . 1.Sensory Neuropathy The most common form of sensory neuropathy is distal symmetric neuropathy, which affects the hands and/or feet bilaterally. Characteristics of distal symmetric neuropathy include loss of sensation, abnormal sensations, pain , and paresthesias . The pain, which is often described as burning, cramping, crushing, or tearing, is usually worse at night and may occur only at that time .

81. The paresthesias may be associated with tingling, burning, and itching sensations. The patient may report a feeling of walking on pillows or numb feet. At times the skin becomes so sensitive (hyperesthesia) that even light pressure from bedsheets cannot be tolerated. Complete or partial loss of sensitivity to touch and temperature is common. Foot injury and ulcerations can occur without the patient ever having pain . Neuropathy can also cause atrophy of the small muscles of the hands and feet, causing deformity and limiting fine movement.

82. 2. Autonomic Neuropathy. Autonomic neuropathy can affect nearly all body systems and lead to hypoglycemic unawareness, bowel incontinence and diarrhea, and urinary retention. Delayed gastric emptying ( gastroparesis ) is a complication of autonomic neuropathy that can produce anorexia, nausea, vomiting, gastroesophageal reflux, and persistent feelings of fullness. Gastroparesis can trigger hypoglycemia by delaying food absorption . Cardiovascular abnormalities associated with autonomic neuropathy are postural hypotension, resting tachycardia, and painless myocardial infarction. A patient with postural hypotension should be instructed to change from a lying or sitting position slowly.

83. Diabetic nephropathy Diabetic nephropathy is the leading cause of end-stage renal disease, accounting for 40% of new cases. The term diabetic nephropathy is used to describe the combination of lesions that often occur concurrently in the diabetic kidney. The most common kidney lesions in people with diabetes are those that affect the glomeruli. Various glomerular changes may occur, including capillary basement membrane thickening, diffuse glomerular sclerosis, and nodular glomerulosclerosis . Among the suggested risk factors for diabetic nephropathy are: Genetic and familial predisposition Elevated blood pressure Poor glycemic control Smoking

84. Pathogenesis Three major histologic changes occur in the glomeruli of persons with diabetic nephropathy. First, mesangial expansion is directly induced by hyperglycemia. Second, GBM (glomerular basement membrane) thickening occurs. Third, glomerular sclerosis is caused by intraglomerular hypertension (induced by renal vasodilatation The exact cause of diabetic nephropathy is unknown, but various postulated mechanisms are: Hyperglycemia (causing hyperfiltration and renal injury) Activation of cytokines

85. Retinopathies Although people with diabetes are at increased risk for the development of cataracts and glaucoma, retinopathy is the most common pattern of eye disease. Diabetic retinopathy is characterized by abnormal retinal vascular permeability, microaneurysm formation, neovascularization ( formation of network with red blood cell ) and associated hemorrhage, scarring, and retinal detachment. Among the suggested risk factors associated with diabetic retinopathy are poor glycemic control, elevated blood pressure, and hyperlipidemia. Because of the risk of retinopathy, it is important that people with diabetes have regular dilated eye examinations. Some people develop a condition called macular edema. It occurs when the damaged blood vessels leak fluid and lipids onto the macula, the part of the retina that lets us see detail. The fluid makes the macula swell, which blurs vision.

86. Pathogenesis Diabetic retinopathy is the result of microvascular retinal changes. Hyperglycemia-induced thickening of the basement membrane lead to incompetence of the vascular walls. These damages change the formation of the blood-retinal barrier and also make the retinal blood vessels become more permeable. The lack of oxygen in the retina causes fragile, new, blood vessels to grow along the retina and in the clear, gel-like vitreous humour that fills the inside of the eye. Without timely treatment, these new blood vessels can bleed, cloud vision, and destroy the retina.

87. Diabetic foot ulcers Foot problems are common among people with diabetes and may become severe enough to cause ulceration and infection, eventually resulting in amputation. Approximately 60% to 70% of people with diabetic foot ulcers have neuropathy without vascular disease, 15% to 20% have vascular disease, and 15% to 20% have neuropathy and vascular disease. Distal symmetric neuropathy is a major risk factor for foot ulcers. People with sensory neuropathies have impaired pain sensation and often are unaware of the constant trauma to the feet caused by poorly fitting shoes, improper weight bearing or infections. Motor neuropathy with weakness of the intrinsic muscles of the foot may result in foot deformities, which lead to focal areas of high pressure. When the abnormal focus of pressure is coupled with loss of sensation, a foot ulcer can occur. Common sites of trauma are the back of the heel, the plantar metatarsal area, or the great toe, where weight is borne during walking.