History and physical examination
Blood tests, including fasting blood glucose, postprandial blood glucose, A1C, lipid profile, blood urea nitrogen and serum creatinine, electrolytes, TSH
Urine for complete urinalysis, microalbuminuria, and acetone (if indicated)
ECG (if indicated)
Funduscopic examination—dilated eye examination
Neurologic examination, including monofilament test for sensation to lower extremities
Ankle-brachial index (ABI) (if indicated)
Foot (podiatric) examination
Monitoring of weight
aspart (Novolo) rapid, 15 min onset, peak 60-90 min (3-4h) EAT
lispro (Humalog) rapid, 15 min onset, peak 60-90 min (3-4h) EAT
glulisine (Apidra) rapid, 15 min onset, peak 60-90 min (3-4h) EAT
regular -short acting Peak 2-3 hr (3-6h) (SQ, IV, IM) only reg IV
NPH -Intermediate action Peak 4-10 hr (10-16h) SQ
detemir (Levemir) - long acting(24h) no pronounced peak, onset 1-2 hr
glargine (Lantus) - long acting(24h) NO DEFINITE PEAK, onset 1-2 hr
(long acting are only SQ)
NEW U-500 REGULAR INSULIN IS NOW AVAILABLE FOR PATIENT WHO ARE ON A HIGH DOSE OF RAPID ACTING INSULIN
RED FLAG, SLOW DOWN, NARROW THERAPEUTIC WINDOW
roll cloudy (NPH)
clear to cloudy
rotate injection sites within major site
• Before loading the syringe, disperse insulin suspensions (ie, NPH insulin preparations) by rolling the vial gently between the palms. Vigorous agitation causes frothing and must be avoided. If granules or clumps remain after mixing, discard the vial.
• Except for NPH insulin, all preparations are formulated as clear, colorless solutions, and hence can be administered without resuspension. If a preparation becomes cloudy or discolored, or if a precipitate develops, discard the vial.
• Before loading the syringe, swab the bottle cap with alcohol.
• Eliminate air bubbles from the syringe and needle after loading.
• Cleanse the skin (with alcohol or soap and water) prior to injection.
• Usual sites of injection are the abdomen, upper arm, and thigh. To minimize variability in responses, make all injections in just one of these areas. Injections in the abdomen provide the most consistent insulin levels and effects.
• Rotate the injection site within the general area employed (eg, the abdomen).
• Allow about 1 inch between sites. If possible, use each site just once a month.
arise from events associated with hyperglycemia and insufficient insulin
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. It is most likely to occur in people with type 1 diabetes but may be seen in type 2 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.
Hyperosmolar hyperglycemic syndrome (HHS) is a life-threatening syndrome that can occur in the patient with diabetes who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion (Fig. 49-12). HHS is less common than DKA. It often occurs in patients over 60 years of age with type 2 diabetes. Common causes of HHS in a patient with type 2 diabetes are infections of the urinary tract, pneumonia, sepsis, any acute illness, and newly diagnosed type 2 diabetes. The main difference between HHS and DKA is that the patient with HHS usually has enough circulating insulin so that ketoacidosis does not occur.
Hypoglycemia, or low blood glucose, occurs when there is too much insulin in proportion to available glucose in the blood. This causes the blood glucose level to drop to less than 70 mg/dL (3.9 mmol/L). Once plasma glucose drops below 70 mg/dL (3.9 mmol/L), neuroendocrine hormones are released and the autonomic nervous system is activated. Suppression of insulin secretion and production of glucagon and epinephrine provide defense against hypoglycemia. Epinephrine release causes manifestations that include shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, and pallor. Because the brain requires a constant supply of glucose in sufficient quantities to function properly, hypoglycemia can affect mental functioning. These manifestations are difficulty speaking, visual disturbances, stupor, confusion, and coma. Manifestations of hypoglycemia can mimic alcohol intoxication. Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death.
Hypoglycemic unawareness is a condition in which a person does not experience the warning signs and symptoms of hypoglycemia until the glucose levels reach a critical point. Then the person may become incoherent and combative or lose consciousness. This is often related to autonomic neuropathy of diabetes that interferes with the secretion of counterregulatory hormones that produce these symptoms. Elderly patients and patients who use β-adrenergic blockers are also at risk for hypoglycemic unawareness.
• Dry mouth
• Abdominal pain* symptom of acidosis
• Nausea and vomiting
• Gradually increasing restlessness, confusion, lethargy
• Flushed, dry skin
• Eyes appear sunken
• Breath odor of ketones
• Rapid, weak pulse
• Labored breathing (Kussmaul respirations)-rapid and deep
• Urinary frequency
• Serum glucose >250 mg/dL (13.9 mmol/L)
• Glucosuria and ketonuria
• Ensure patent airway.
• Administer oxygen via nasal cannula or non-rebreather mask.
• 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.
• 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).
pathophysiologic processes of diabetic neuropathy are not well understood. Several theories exist, including metabolic, vascular, and autoimmune elements.
The prevailing theory suggests that persistent hyperglycemia leads to an accumulation of sorbitol and fructose in the nerves that causes damage by an unknown mechanism. The result is reduced nerve conduction and demyelinization.
Ischemia in blood vessels damaged by chronic hyperglycemia that supply the peripheral nerves is also implicated in the development of diabetic neuropathy.
Neuropathy can precede, accompany, or follow the diagnosis of diabetes
Control of blood glucose is the only treatment for diabetic neuropathy, being effective in many, but not all cases
Sensory neuropathy is a major risk factor for lower extremity amputation in the person with diabetes.
Autonomic neuropathy can affect nearly all body systems and lead to hypoglycemic unawareness, bowel incontinence and diarrhea, and urinary retention.
Erectile dysfunction (ED) in diabetic men is well recognized and common, often being the first manifestation of autonomic failure
PAD increases the risk for amputation by causing a reduction in blood flow to the lower extremities.
When blood flow is decreased, oxygen, white blood cells, and vital nutrients are not available to the tissues.
Therefore wounds take longer to heal and the risk for infection increases.
Signs of PAD include intermittent claudication, pain at rest, cold feet, loss of hair, delayed capillary filling, and dependent rubor (redness of the skin that occurs when the extremity is in a dependent position).
The disease is diagnosed by history, ankle-brachial index (ABI), and angiography.
Management includes control or reduction of risk factors, particularly smoking, high cholesterol intake, and hypertension. Bypass or graft surgery is indicated in some patients.
Proper care of the feet is essential for the patient with PAD
1. Wash feet daily with a mild soap and warm water. First test water temperature with hands.
2. Pat feet dry gently, especially between toes.
3. Examine feet daily for cuts, blisters, swelling, and red, tender areas. Do not depend on feeling sores. If eyesight is poor, have others inspect feet.
4. Use lanolin on feet to prevent skin from drying and cracking. Do not apply between toes.
5. Use mild foot powder on sweaty feet.
6. Do not use commercial remedies to remove calluses or corns.
7. Cleanse cuts with warm water and mild soap, covering with clean dressing. Do not use iodine, rubbing alcohol, or strong adhesives.
8. Report skin infections or nonhealing sores to health care provider immediately.
9. Cut toenails evenly with rounded contour of toes. Do not cut down corners. The best time to trim nails is after a shower or bath.
10. Separate overlapping toes with cotton or lamb's wool.
11. Avoid open-toe, open-heel, and high-heel shoes. Leather shoes are preferred to plastic ones. Wear slippers with soles. Do not go barefoot. Shake out shoes before putting on.
12. Wear clean, absorbent (cotton or wool) socks or stockings that have not been mended. Colored socks must be colorfast.
13. Do not wear clothing that leaves impressions, hindering circulation.
14. Do not use hot water bottles or heating pads to warm feet. Wear socks for warmth.
15. Guard against frostbite.
16. Exercise feet daily either by walking or by flexing and extending feet in suspended position. Avoid prolonged sitting, standing, and crossing of legs.
is characterized by insulin resistance, elevated insulin levels, high levels of triglycerides, decreased levels of high-density lipoproteins (HDLs), increased levels of low-density lipoproteins (LDLs), and hypertension.
Risk factors for metabolic syndrome include, but are not limited to, central obesity, sedentary lifestyle, urbanization/Westernization, and certain ethnicities (Native Americans, Hispanics, and African Americans).
Overweight individuals with metabolic syndrome can prevent or delay the onset of diabetes through a program of weight loss and regular physical activity.