Wk 10. Management of Clients with Diabetes Mellitus

Transcription

1 Wk 10. Management of Clients with Diabetes Mellitus 2. Acute complications of DM 1) Hyperglycemia and diabetic ketoacidosis Hyperglycemia: glycogenolysis gluconeogenesis 1) Etiology and Risk Factors Taking too little insulin Skipping doses of insulin 2) Pathophysiology Diabetic ketoacidosis relative or absolute lack of insulin Excess production of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormones) antagonize effects of insulin and foster (1) Ketosis and Acidosis In diabetic ketoacidosis, fail to compensate for ketosis (2) Dehydration excrete large amounts of urine to eliminate excessive glucose and ketones severe nausea and vomiting (3) Electrolyte Imbalance Acidosis: accumulating hydrogen ions from ECF to ICF promotes move of potassium from ICF to ECF 2) Clinical Manifestations Common Manifestations Abdominal pain Anorexia Dehydration Fruity odor of ketones on breath Hyperpnea or Kussmaul s respirations Hypotension Impaired level of consciousness or coma Nausea and vomiting Polyuria Somnolence Tachycardia Thirst Visual disturbances Warm, dry skin Weakness Weight loss Priority Assessments for Acute Hyperglycemia Dehydration Assess skin for dryness, flushed color, tenting. Assess mucous membranes for dryness. Monitor urine output for polyuria followed by oliguria. Monitor vital signs for hypotension, tachycardia. Fluid overload during treatment for hyperglycemia. Electrolyte Monitor for hyperkalemia: peaked T waves on ECG, imbalances changes in heart rate, hypotension, diarrhea and hyperactive bowel sounds, muscle cramps, nausea and vomiting, hypotension. Monitor for hypokalemia: flattened T waves on ECG, hypotension, ileus, nausea and vomiting,fatigue, lethargy, muscle weakness and cramps. Monitor for hyponatremia: nausea, vomiting, diarrhea, tachycardia, hypotension, lethargy, confusion, seizures, muscle weakness. Hyperglycemia Monitor blood glucose levels and check urine for ketones. Monitor for polyuria, polyphagia, and polydipsia. Monitor for hypoglycemia during treatment for hyperglycemia. Hyperosmolality Monitor serum osmolality, blood urea nitrogen,serum creatinine. Assess for lethargy, disorientation, and behavioral

2 Metabolic acidosis changes. Monitor for hypotension, dysrhythmias, hyperventilation, lethargy, confusion, coma, headache, acetone breath 3) Medical Management Management in diabetic ketoacidosis rehydration correction of electrolyte and acidbase imbalances (1) Rehydrate Intravenous rehydration: Immediate IV of isotonic or N/S (0.9% sodium chloride) During the first hour: 1000 ml of isotonic solution (10 to 20 ml/kg) next 24 hours: additional 2000 to 8000 ml of solution (2) Restore Potassium Balance Lower potassium in ICF temporary hyperkalemia total body potassium level depleted Correct potassium replacement with caution Assessessment hyperkalemia: bradycardia, cardiac arrest, weakness, flaccid paralysis, oliguria during first 4 hours of intervention hypokalemia: weakness, flaccid paralysis, paralytic ileus, cardiac arrest 4 to 24 hours after initial intervention Replace potassium carefully following protocols (3) Correct ph and Administer Insulin phosphate depletion: decreased food intake, excessive catabolism, increased urinary excretion potassium with insulin: movement of phosphate into cells reduces plasma phosphate concentration too much phosphate hypocalcemia Calcium check before phosphate (as potassium phosphate) is given sodium bicarbonate only when blood ph < 7.1 Low-dosage insulin therapy (5 to 10 units/hour) Never give SQ in diabetic ketoacidosis After bolus, infuse insulin (0.1 unit/kg/hour) no improvement of acidosis within 2 ~ 4 hrs double infusion rate glucose normalized more quickly than ph Monitor blood glucose every 30 mins initially blood glucose : 250 mg/dl reduce insulin infusion and add 5% dextrose Before stopping IV insulin(15~30 mins), shortacting insulin SQ every 4~6 hrs initial SQ dose: 0.2 unit/kg

3 (4) Prevent Recurrence Primary prevention: patient education for preventing diabetic ketoacidosis Take insulin in appropriate doses at appropriate times Patients should telephone for assistance when ~ Anorexia, nausea, vomiting, or diarrhea 2) Hyperglycemic hyperosmolar nonketotic syndrome HHNS major difference from DKA: lack of ketonuria 4 major clinical features of HHNS Severe hyperglycemia (600 to 2000 mg/dl) No or only slight ketosis Profound dehydration (10% to 15% loss of body water) Treatment fluid replacement and administration of insulin and electrolytes initially: infusion of N/S over a 2-hour period hypotonic (0.45%) saline IV correction of potassium, sodium, chloride, phosphates Lower dosage insulin via infusion pump Careful assessment needed: older, other cardiovascular or renal disorders, acute or chronic renal failure 3) Hypoglycemia Known as insulin reaction or hypoglycemic reaction, common in type 1 Blood glucose < 50 to 60 mg/dl 1) Etiology and Risk Factors Insulin and sulfonylurea overdose Omitting a meal or eating less food than usual > age 60 years taking oral hypoglycemic with poor intake, use alcohol, hepatic or renal dysfunction 2) Pathophysiology Glucagon secretion deficiency epinephrine impaired secondary to subclinical neuropathy Impaired insulin absorption from SQ fat 2) Clinical Manifestations (1) Adrenergic Adrenergic (autonomic) symptoms mild reactions Diaphoresis: adrenergic symptom of hypoglycemia (2) Neuroglycopenic symptoms

4 Associated with lack of glucose availability in brain decrease in cognitive functioning longer lasting, more severe headache, irritability, drowsiness, weakness, tremor Pts may be awake and alert, semicomatose, comatose 3) Medical Management (1) Return Blood Glucose to Normal mild hypoglycemia: 15 g of simple carbohydrate Reactions during night: carbohydrate longer-acting mixture of CHO and protein (230ml of milk) hypoglycemia in hospital 10 to 25 g of IV glucose (as 50% or 25% dextrose) over 1 to 3 mins IV infusion of 5% dextrose at 5 ~10 g/hour until fully recovered (2) Prevent Hypoglycemia Why hypoglycemia occurs When it is most likely to occur early clinical manifestations of hypoglycemia danger of severe or repeated reactions importance of early intervention How to prevent insulin reactions diabetic identification tag, medical identification bracelet or necklace, diabetic identification card 3. Other hypoglycemic disorders 1) Hypoglycemic Unawareness Repeated episodes of hypoglycemia blunt hormonal defense mechanisms (blunted epinephrine response) Contradication: beta-blockers Beta-blockers (propranolol) hypoglycemic unawareness and blunt adrenergic (epinephrine) effects hypoglycemic unawareness (glucose < 55 mg/dl) need consultation 2) Hypoglycemia with Rebound Hyperglycemia (Somogyi Effect) Hypoglycemia with rebound hyperglycemia: Somogyi effect or phenomenon common cause of fasting morning hyperglycemia <pathophysiology> hypoglycemia counterregulatory hormone secretion, resultant liver production of glucose increase glucose, with insulin resistance secondary to increased hormone rebound hyperglycemia If early-morning < 50 to 60 mg/dl, 7:00 AM > 180 to 200 mg/dl <Prevention> Decreasing intermediate-acting insulin dose at dinner time or moving intermediate-acting insulin dose to bedtime or increasing size of bedtime snack

5 3) Dawn Phenomenon early-morning (4 to 8 AM) blood glucose increase without preceding nocturnal hypoglycemia possible causes Growth hormone, increased insulin clearance early-morning hypoglycemia to normalize prebreakfast glucose Ultralente > NPH insulin 5. Chronic complications of diabetes mellitus major causes of morbidity and mortality in DM patients - Macrovascular: coronary artery disease, cerebrovascular disease, hypertension, peripheral vascular disease, and infection - Microvascular: retinopathy, nephropathy, neuropathy 1) Macrovascular complications Coronary artery disease, cerebrovascular disease, and peripheral vascular disease tend to occur at earlier age Atherosclerosis type 1 > type 2 most common cause of death in DM, 40% ~ 60% of all DM complication syndrome X : tends to occur years before onset of clinical DM Health promotion activities managing obesity and maintaining ideal body weight exercising not smoking achieving normal blood lipid levels <Coronary Artery Disease> 2~4 times more likely to die of CAD 3~4 times greater relative risk factor for cardiovascular disease in women with type 2 insulin therapy in type 2 recommended actually increase incidence of atherosclerotic disease leads to weight gain, increased blood pressure <Cerebrovascular Disease> Prevention control of hypertension, lipid levels, and obesity smoking cessation exercise good nutritional practices <Hypertension> 40% increased rate of hypertension major risk factor for stroke and nephropathy

6 pharmacologic treatment for hypertension >130/80 mm Hg Angiotensin- converting enzyme (ACE) inhibitors calcium-channel blockers (CCB) Beta-blockers and diuretics: increase glucose tolerance and lipid levels <Peripheral Vascular Disease> bruits, intermittent claudication, absent pedal pulses, ischemic gangrene ½ nontraumatic lower limb amputations sensory,autonomic neuropathy, peripheral vascular disease increased risk and rate of infection, poor healing <Infections> susceptible to infections, difficult to treat 3 factors impaired polymorphonuclear leukocyte function diabetic neuropathies vascular insufficiency 2) Microvascular complications changes in retinal, renal, and peripheral capillaries <Diabetic Retinopathy> major cause of blindness about 80%: retinopathy 15 years after diagnosis probably associated with protein glycosylation, ischemia, hemodynamic mechanisms increased blood viscosity, increases permeability, decreases elasticity of capillaries when acute vision problems Blurred vision: common from an abnormally high blood glucose seeing floaters or flashing lights : hemorrhage, retinal detachment Major interventions in early phases: achievement of euglycemia, normalization of BP <Nephropathy> OPD laser therapy (photocoagulation) Vitrectomy: surgical procedure to removes vitreous and replaces with saline solution single most common cause of stage 5 chronic kidney disease formerly known as ESRD self-check microalbumin levels at home detect very small quantities of urinary albumin: very early renal disease unsuccessfully treated nephropathy stage 5 chronic kidney disease : known as ESRD hemodialysis, peritoneal dialysis, or kidney transplantation <Neuropathy> most common chronic complication

7 Nearly 60% mononeuropathy or polyneuropathy sensory or motor impairment nerve pain different from other types of pain numbness, stabbing, tingling, or burning sensation diabetic peripheral neuropathy (DPN) <Mononeuropathy> focal neuropathy, usually involves a single nerve or group of nerves sharp, stabbing pains caused by an infarction of the blood supply <Polyneuropathy> diffuse neuropathy, sensory and autonomic nerves Sensory neuropathy : most common type Polyneuropathy: may simply resolve spontaneously. <Autonomic Neuropathy> effect on pupillary, cardiovascular, gastrointestinal, genitourinary functions Pupillary Autonomic neuropathy of pupil interferes with pupil s ability to adapt to the dark Cardiovascular Autonomic neuropathy of the cardiovascular system Gastrointestinal dysphagia, abdominal pain, nausea, vomiting, malabsorption postprandial hypoglycemia, diarrhea, constipation, fecal incontinence Genitourinary Bladder hypotonicity, neurogenic bladder straining with urination, infrequent urge to urinate, decreased urine stream Urinary stasis UTI