Medical Surgical Care Plan On Patients With Diabetes Mellitus.

PATHOPHYSIOLOGY

Diabetes mellitus (DM) is a worldwide epidemic of chronic hyperglycemia affecting more than 7.8% (24 million) of the total U.S. population. There are 1.6 million new cases of DM diagnosed in the United States each year. While 18 million cases are diagnosed, more than 6 million remain undiagnosed. An additional 57 million Americans are at risk of DM.

Hispanic, Native American, and African American populations have a higher incidence than Caucasians and other groups and are the most likely to be undiagnosed. Prevalence has increased in a direct relationship with increasing incidence of obesity.

Metabolic, vascular, and neurologic disorders ensue from dysfunctional glucose transport into body cells. Insulin facilitates glucose transport into cells for oxidation and energy production.

Food intake, glycogen breakdown, and gluconeogenesis increase the serum glucose level, which stimulates the beta islet cells of the pancreas to release needed insulin for transport of glucose from the bloodstream into the cells. At the cellular level, insulin receptors control the rate of transport
of glucose into the cells.

As glucose leaves the blood, serum levels return to normal (70-100 mg/dL). Individuals with DM have impaired glucose transport
because of decreased or absent insulin secretion and/or ineffective
insulin receptors. Carbohydrate, fat, and protein metabolism are abnormal, and patients are unable to store glucose in the liver and muscle as glycogen, store fatty acids and triglycerides in adipose tissue, or transport amino acids into cells normally.

DM is classified into the following four clinical classes including prediabetes.

Type 1 (5%-10%): Complete lack of effective endogenous insulin, causing hyperglycemia and ketosis resulting from beta islet cell destruction. This type is precipitated by altered immune responses, genetic factors, and environmental stressors. Certain human leukocyte antigens have been strongly associated with type 1 DM. These individuals depend on
insulin for survival and prevention of life-threatening diabetic ketoacidosis (DKA).

Type 2 (90%-95%): Metabolic disorder that may range from insulin resistance with moderate insulin deficiency to a severe defect in insulin secretion with insulin resistance that results in severe hyperglycemia without ketosis. Untreated hyperglycemia can result in hyperglycemic hyperosmolar syndrome (HHS). Most individuals with type 2 DM are obese.

Other types: Formerly termed secondary diabetes, these include the following:

• Diseases of the exocrine pancreas: Pancreatitis, cystic fibrosis, hemochromatosis, trauma, infection, pancreatic cancer, and pancreatectomy may result in destruction of beta islet cells. All diseases except cancer generally involve extensive pancreatic destruction.

• Drug-induced by insulin antagonists: Many drugs impair
insulin secretion, including phenytoin, steroids (hydrocortisone,
dexamethasone), hormones (estrogen), intravenous (IV) pentamidine, nicotinic acid, thyroid hormone, thiazides, alpha-interferon, and rat poison.

• Endocrine dysfunction/hormonal diseases: Growth hormone, epinephrine, cortisol, and glucagons antagonize insulin and may be increased when diseases such as acromegaly, Cushing’s syndrome, pheochromocytoma, or glucagonoma are present. Presence of excess antagonistic hormones results in reduced insulin action, and with somatostatinoma and aldosteronoma, insulin secretion may be reduced.

• Genetic defects of the beta cell: An autosomal dominant pattern results in severely impaired insulin secretion, most often characterized by hyperglycemia beginning before 25 years of age; it is also termed maturity onset diabetes of the young.

• Genetic defects in insulin action: A genetic defect manifested as abnormal insulin action is reflected by hyperinsulinemia with mild to severe hyperglycemia. Persons with acanthosis nigricans and women with polycystic ovaries may have this type of insulin resistance. Leprechaunism and Rabson- Mendenhall syndrome are two pediatric syndromes in this
category.

• Infections: Presence of several different viruses, including rubella, coxsackievirus B, cytomegalovirus (CMV), adenovirus, and mumps has resulted in beta cell destruction.

• Uncommon immune-mediated diabetes: Antiinsulin receptor antibodies bind to insulin receptors and can either block or increase binding of insulin, resulting in either hyperglycemia or hypoglycemia. Systemic lupus erythematosus and “stiff-man” syndrome are examples of implicated disorders.

• Other genetic syndromes: Hyperglycemia has been linked to patients with Down’s syndrome, Klinefelter’s syndrome, Turner’s syndrome, and Wolfram’s syndrome.

Many of these “secondary” causes have recently become subclassified under type 1 and type 2 DM as possible primary causes of these diseases.

Gestational diabetes mellitus (GDM): Glucose intolerance with hyperglycemia that develops during pregnancy in approximately 4% of pregnant women, resulting in increased perinatal risk to the child and increased risk (25%) of the mother developing chronic DM during the next 10-15 yr. This type does not include previously diabetic pregnant women. Deterioration of glucose tolerance is considered “normal” during the third trimester of pregnancy.

Prediabetes with impaired glucose tolerance and impaired fasting glucose: Certain individuals may manifest chronic hyperglycemia without meeting other criteria for DM and are classified as having impaired glucose tolerance (IGT) or impaired fasting glucose (IFG), with fasting blood glucose levels 100 mg/dL or more but less than 126 mg/dL or 2-hr oral
glucose tolerance test (OGTT) of 140 mg/dL or more but less than 200 mg/dL.

These persons are at risk for developing DM and cardiovascular disease. IGT was formerly termed borderline, chemical, latent, subclinical, or asymptomatic DM. At least 20.1 million people in the United States, ages 40 to 74, have prediabetes. Some long-term damage to the body, especially
the heart and circulatory system, already may be occurring during prediabetes. If blood glucose is controlled when prediabetes is identified, development of type 2 DM can be prevented.

ASSESSMENT

Metabolic signs of chronic hyperglycemia: Fatigue, weakness, weight loss, paresthesias, mild dehydration, and symptoms of hyperglycemia (polyuria, polydipsia, polyphagia).

These indicators are seen in the early stages of illness.

Impending type 1 crisis—DKA: Profound dehydration and hyperglycemia, electrolyte imbalance, metabolic acidosis caused by ketosis, altered mental status, Kussmaul’s respirations (paroxysmal dyspnea), acetone breath, possible hypovolemic shock (hypotension, weak and rapid pulse), abdominal pain, and possible strokelike symptoms.

Impending type 2 crisis—HHS: Severe dehydration, hypovolemic
shock (hypotension, weak and rapid pulse), severe hyperglycemia, shallow respirations, altered mental status, slight lactic acidosis or normal pH, possible strokelike symptoms.

COMPLICATIONS

Potential for acute crisis: For type 1, include DKA and hypoglycemia; for Type 2, include HHS and hypoglycemia. All individuals with DM are at higher risk for developing cardiovascular disease. These complications should be preventable and are discussed as follows.

Long-term complications: The most important factor in delaying progression to long-term complications is stabilization of blood glucose levels to normal range.

Macroangiopathy: Patients are at higher risk for heart attack and stroke caused by vascular disease affecting the coronary arteries and larger vessels of the brain and lower extremities (peripheral vascular disease [PVD]). Risk
factors are hyperglycemia, hypertension, hypercholesterolemia,
smoking, aging, and extended duration of DM.

Microangiopathy: Patients are at higher risk for blindness and renal failure caused by thickening of capillary basement membranes resulting in retinopathy and nephropathy. Early symptoms include increased leakage of retinal vessels and microalbuminuria.

Neuropathy: Patients are at higher risk for gastroparesis (impaired gastric emptying), lack of sensation (especially in the feet), and neurogenic bladder caused by deterioration of peripheral and autonomic nervous systems, resulting in impaired or slowed nerve transmission.

Nursing Diagnosis:

Risk for Unstable Blood Glucose Level: related to inadequate blood glucose monitoring, dietary intake, and/or medication management.

Desired Outcomes: Optimally, the patient has a blood glucose reading of less than 180 mg/ dL at all times; fasting blood glucose readings less than 140 mg/dL when hospitalized; hemoglobin A1C level of less than 7; adequate tissue perfusion as evidenced by warmth, sensation, brisk capillary refill time (less than 2 sec), and peripheral pulses greater than 2+ on a 0-4+ scale in the extremities; BP within his or her optimal range; urinary output 30 mL/hr or more; baseline vision; good appetite; and absence of nausea and vomiting. The patient demonstrates adherence to the therapeutic regimen (essential for promoting optimal tissue perfusion).

Nursing Interventions	Rationales
Assess blood glucose before meals and at bedtime.	This monitors effectiveness of blood glucose control at times when the patient’s glucose is not increased by food being digested.
Assess for changes in mentation, apprehension, erratic behavior, trembling, slurred speech, staggering gait, and seizure activity. Treat hypoglycemia as prescribed.	These are signs of hypoglycemia. Patients with hypoglycemia may experience vasodilation and diminished myocardial contractility, which decrease cerebral circulation and impair cognition.
In addition to sensation, assess capillary refill, temperature, peripheral pulses, and color.	This assessment monitors the patient’s peripheral perfusion to detect macroangiopathy or PVD.
Administer basal, prandial, and correction doses of insulin as prescribed.	Adherence to the therapeutic regimen is essential for promoting optimal tissue perfusion. Progression of vascular disease and neuropathy, including blindness, kidney failure, gastroparesis, heart attack, and stroke, is the root cause of all complications of DM. By keeping serum glucose in a more normal range, the vascular endothelium receives better nourishment within the cells and will be less likely to deteriorate.
Encourage and teach the patient how to perform regular home blood glucose monitoring.	Blood glucose is generally monitored before meals, at bedtime, and possibly during the night (3:00 AM) in order to assess whether a correction dose of short-acting insulin is needed. Self-monitoring by patients is extremely useful in reducing complications.
Check BP every 4 hr. Alert the health care provider to values outside the patient’s normal range. Administer antihypertensive agents as prescribed and document response.	Hypertension is commonly associated with diabetes. Careful control of BP is critical in preventing or limiting development of heart disease, stroke, retinopathy, and nephropathy.
Monitor for orthostatic hypotension after administering blood pressure medications. For more information, see discussion later in this nursing diagnosis.	Orthostatic hypotension is a potential side effect of antihypertensive agents and of autonomic neuropathy in which the patient’s compensatory mechanisms may be impaired.
Teach the patient to avoid pressure at the back of the knees by not crossing legs or “gatching” bed under the knees. Caution the patient to avoid garments that constrict circulation to the extremities and lower body.	These actions could cause venous stasis and reduction in arterial perfusion in patients with macroangiopathy or impending PVD.

Nursing Diagnosis:

Risk for Infection: related to chronic disease process (e.g., hyperglycemia, neurogenic bladder, poor circulation)

Desired Outcome: The patient is asymptomatic for infection as evidenced by normothermia, negative cultures, and white blood cell count 11,000/mm3 or less.

Nursing Interventions	Rationales
Assess temperature every 4 hr. Alert the health care provider to elevations.	Infection is the most common cause of DKA. Fever can signal presence of an infection.
Maintain meticulous sterile technique when changing dressings, performing invasive procedures, or manipulating indwelling catheters.	Nonintact skin and invasive procedures and catheters place patients at risk for ingress of bacteria.
Monitor for indicators of infection, including the following: Fever, chills, cough productive of sputum, crackles, rhonchi, dyspnea, inflamed pharynx, and sore throat.	These are indicators of upper respiratory infection.
Burning or pain with urination, cloudy or malodorous urine, tachycardia, diaphoresis, nausea, vomiting, and abdominal pain.	These are indicators of urinary tract infection (UTI). Patients with DM often have a neurogenic bladder, which increases the chance of UTI caused by urinary retention.
Hypothermia, flushed skin, and hypotension. Erythema, swelling, purulent drainage, and warmth at IV sites.	These are indicators of systemic sepsis. These are indicators of localized infection.
Consult the health care provider about obtaining culture specimens for blood, sputum, and urine during temperature spikes or for wounds that produce purulent drainage.	Infection can be present in blood (sepsis), urine, sputum (lungs/ respiratory tract), or wounds. Occult infection also can be present outside these sources.

Nursing Diagnosis:

Risk for Impaired Skin Integrity: related to altered circulation and sensation occurring with peripheral neuropathy and vascular pathology.

Desired Outcomes: The patient’s lower extremity skin remains intact. Within the 24-hr period before hospital discharge, the patient verbalizes and demonstrates knowledge of proper foot care.

Nursing Interventions	Rationales
Assess integrity of the skin and evaluate reflexes of the lower extremities by checking knee and ankle deep tendon reflexes, proprioceptive sensations, two-point discrimination, and vibration sensation (using a tuning fork on the medial malleolus).	These assessments monitor presence/degree of neuropathy and vascular pathology. In addition to higher-risk areas on the extremities and pressure points, skin on the legs is at highest risk and typically is the first to exhibit problems. If sensations are impaired, the patient likely will be unable to respond appropriately to stimuli.
Monitor peripheral pulses, comparing quality bilaterally.	Peripheral pulses 2+ or less on a 0-4+ scale signal poor circulation that could compromise skin integrity.
Use a foot cradle on the bed, space boots for ulcerated heels, elbow protectors, and pressure-relief mattress.	These measures prevent pressure points and promote patient comfort.
Minimize patient activities and incorporate progressive passive and active exercises into the daily routine. Discourage extended rest periods in the same position.	These measures alleviate acute discomfort while preventing hemostasis.
Teach the patient the following steps for foot care: Wash feet daily with mild soap and warm water; check water temperature with water thermometer or elbow.	Patients with decreased sensation are at risk for burns if they are unaware that water temperature is too hot. Hot water and strong soaps also can promote dry skin, which can become irritated and break down.
Inspect feet daily for the presence of erythema, discoloration, or trauma, using mirrors as necessary for adequate visualization.	These are signs the skin needs vigilant assessment and preventive care. When the skin is no longer intact, the patient is at risk for infection that eventually can lead to amputation.
Change socks or stockings daily and wear white cotton or wool blends.	These measures prevent infection from moisture or dirt in contact with nonintact skin. The white fabric enables patients more readily to see any blood or exudates from nonintact skin.
Attend to any foot injury immediately, and seek medical attention.	Diabetes can cause slow wound healing. Prompt care can prevent a small injury from becoming worse.

Nursing Diagnosis:

Deficient Knowledge: related to unfamiliarity with proper insulin administration, dietary precautions, and exercise for promoting normoglycemia

Desired Outcome: Within the 24-hr period before hospital discharge, the patient verbalizes and demonstrates knowledge of proper insulin administration, symptoms and treatment of hypoglycemia, the prescribed dietary regimen, and the role of exercise in promoting normoglycemia.

Nursing Interventions	Rationales
Assess the patient’s health care literacy (language, reading, comprehension). Assess culture and culturally specific information needs.	This assessment helps ensure that information is selected and presented in a manner that is culturally and educationally appropriate.
Teach the patient to check expiration date on the insulin vial and to avoid using it if outdated.	Insulin may lose potency if the bottle has been open for more than 30 days.
Also teach proper storage of insulin and the importance of avoiding temperature extremes.	Extreme temperatures destroy insulin.
Teach the patient to use U-100 insulin with U-100 syringes as needed. Insulin pens are preferred to use of insulin syringes.	The patient must be aware there are differences in strengths of insulin suspensions, and each strength must be given using the appropriate syringe.
Suggest that the patient ask his or her health care provider if the prescribed insulin is available in an insulin pen.	An insulin pen eliminates the chance for errors since the pen is a self-enclosed dosing system, wherein the patient applies a new needle and sets the dose using a dial on the pen.
Explain that some intermediate- and long-acting insulins require mixing. Demonstrate rolling the insulin vial between your palms to mix contents.	Insulin separates when the bottle sits, and the molecules must be remixed to ensure appropriate concentration throughout the vial.
Explain that long-acting analogue insulins (glargine/Lantus and detemir/Levemir) work differently from older long-acting insulins and may need to be administered only once or twice daily, depending on the dose.	Long-acting insulin analogues do not have a profound peak action. Once glargine is injected and absorbed, the action is consistent over 24 hr, while the duration of action of detemir is approximately 20 hr.
Caution the patient to avoid shaking the vial of insulin.	Shaking produces air bubbles that can interfere with accurate dose measurement.