DIABETIC KETOACIDOSIS (DKA) September 14, 2012 An acute complication of DM is characterized by: 1. Hyperglycemia 2. Ketonuria 3. Acidosis 4. Dehydration 1. Insulin deficiency prevents glucose from being used for energy, forcing the body to metabolize fat for fuel. 2. Free fatty acids, released from the metabolism of fat are converted to ketone bodies in the liver. 3. Ketone bodies are organic acids that cause metabolic acidosis. 4. Osmotic diuresis caused by hyperglycemia creates a shift in electrolytes, with losses in potassium, sodium, phosphate, and water. Clinical Manifestations Early Stage Late Stage Poly-dipsia,uria Kussmaul respirations Fatigue, malaise, Fruity, sweet breath drowsiness Hypotension, weak pulse Anorexia, N/V Stupor and coma Abdominal pains, muscle cramps Diagnostic Evaluation 1. Serum glucose elevated over 300mg/dL – 1000mg/dL 2. Serum and urine ketone bodies (+) 3. Serum Na and K = low, normal or high 4. Serum HCO3 and pH = decreased = pCO2 5. BUN, creatinine, hemoglobin, and hematocrit = elevated 6. Urine glucose (+) in high concentration, Specific Gravity is increased. Nursing Interventions - Assess for signs of dehydration - MIO - Monitor urine specific gravity and blood glucose - Assess for symptoms of hypokalemia. Administer replacement electrolytes and insulin as ordered. - Monitor serum glucose, bicarb, and pH levels - Provide reassurance about the improvement of condition and that correction of fluid imbalance will help reduce discomfort. Management: - IV fluids for fluid replacement (PNSS) - IV insulin drip (regular insulin) - Electrolyte replacement -
HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME (HHNS) - An acute complication of DM2 characterized by hyperglycemia, dehydration, and hyperosmolarity, but with little or no ketones Pathophysiology: 1. Prolonged hyperglycemia with glucosuria produces osmotic diuresis 2. Loss of H2O, Na and K results in severe dehydration, causing hypovolemia and hemoconcentration. 3. Hyperosmolarity d/t increased glucose and sodium 4. Isulin continues to be produced at a level that prevents ketosis. 5. Increased blood viscosity causes tissue hypoxia. 6. Caused by incadequate amount of endogenous/exogenous insulin to control hyperglycemia. o Use of therapeutic agents increase blood glucose levels (glucocorticoids, immunosuppressive agents) o Use of therapeutic procedures that cause stress or increase blood glucose levels (hyperosmolar hyperalimentation, peritoneal dialysis) Clinical Manifestation Early Stage Late Stage Polyuria, degydration Stupor and coma, seizures Fatigue, malaise, Muscle weakness N/V Diagnostic Examination - Serum glucose and osmolality = elevated - Serum and urine ketone bodies = minimal to absent - Serum Na and K levels = may be elevated - BUN and creatinine = may be elevated - Urine specific gravity = elevated Management 1. Correct fluid and electrolyte imbalances with IV fluids 2. Provide insulin via IV drip to lower plasma glucose 3. Evaluate complications, such as stupor, seizures, or shock, and treat appropriately 4. Identify and treat underlying illnesses or events that precipitate HHNS Complications 1. Too rapid infusion IV fluids can cause cerebral edema and death 2. HHNS is a medical emergency that, in not treated properly, can cause death 3. Patients who become comatose will need nasogastric tubes to prevent aspiration. Criteria Age S/Sx PA Diags Onset Mortality DKA Any age 3P’s, orthopneic hypotension, LOC changes, N/V Dry flushed skin, poor turgor, dec BP, dry mucous membrance, Kuss respi and acetone breath Glucose, Ketones (+), BUN, Crea, WBC Hours to days <10 HHS >50 yrs DKA, but has slower onset Same with DKA but w/o Kuss and acetone breath Ketones absent, WBC normal with inf Days to weeks 10-25%
PHEOCHROMOCYTOMA - A benign tumor
Originates from the chromaffin cells of the adrenal medulla 80-90%, tumor in the medulla May occur at any age (peak: 40 and 50 years) Affects men and women equally High incidence in family members 10% are malignant
Clinical Manifestation - Typical triad of symptoms: headache, diaphoresis, and palpitations - HPN and cardiovascular disturbances - Tremor, headache, flushing, and anxiety - Hyperglycemia results from glycogenolysis (may need insulin to control glucose levels) - Acute, unpredictable attacks: seconds to hours duration - Manifestations: extremely anxious, weak, headache, vertigo, blurring of vision, tinnitus, air hunger, and dyspnea, polyuria, N/V, diarrhea, abdominal pain, and a feeling of impending doom. - Palpitations and tachycardia - BP exceeds 250/150 mmHg Assessment: 5H’s (Hypertension, Headache, Hyperhidrosis (excessive sweating), Hypermetabolism, Hyperglycemia) Diagnostic Examinations - Urinary catecholamine metabolites measurements (metanephrines [MN] and vanillylmandelic acid [VMA]) or free catecholamines - 24-hour urine specimen - Medications and foods (coffee, tea, bananas, chocolate, vanilla, aspirin) may alter results of these tests - Anti HPN drugs are not given prior to testing of urine - CT scans, MRI, and UTZ to localize disease and to assess number of tumors - 131I-metaiodobenzylguanidine (MIBG) scintigraphy: determines location of tumor and metastasis - MIBG: a specific isotope for catecholamine-producing tissue - MIBG scinitgraphy is: noninvasive, safe has increased the accuracy of diagnosing tumors - Histamine Test: Histamine is administered, if BP rises after a minute (+), standard BP at baseline (170/110 and below only); Regitine test: decreases BP 1-3 minutes, at least 35mmHg (+) Management - Patient is placed on bed rest with the head of the bed elevated to promote an orthostatic decrease in blood pressure - ICU for monitoring of ECG - Administration of alpha-adrenergic blocking agents or smooth muscle relaxants to lower BP - Phenoxybenzamine (Dibenzyline), long-acting alpha-blocker if BP is stable for surgery - Beta-adrenergic blocking agents used in patients with dysrhythmias - Hypotension and hyperglycemia may occur post-OP - Manipulation of glands during surgery - Corticoid therapy
CHRONIC RENAL FAILURE - A large number of nephrons are damaged due to acute or chronic kidney disease - Nephrons die off, the undamaged ones increase their work capacity - Patient may have significant kidney damage without showing symptoms of renal failure Causes: - Hypertension (prolonged and severe) - DM - Glomerulopathies (from SLE and other disorders) - Nephritis - Hereditary renal disease - Obstructive uropathy - Developmental or congenital disorders Consequences 1. Progression varies on underlying cause and severity 2. Stages: decreased renal reserve, renal insufficiency, renal failure, ESRD 3. Retention of Na and H2O 4. Decreased GFR (RAAM) 5. Metabolic acidosis 6. Decreased GFR increases phosphate, with reciprocal decrease in serum Ca and bone reabsorption of Ca 7. Erythropoietin decreases 8. Uremia affects CNS Clinical Manifestations 1. GI: anorexia, N/V, hiccups, ulcers and hemorrhage 2. Cardiovascular: hyperkalemia, HPN, pericarditis, pericardial effusion and tamponade 3. Respiratory: pulmonary edema, pleural effusions and rub 4. Neuromuscular: fatigue, sleep disorders, headache, lethargy, muscular irritability, peripheral neuropathy, seizures, coma 5. Metabolic and endocrine: glucose intolerance, hyperlipidemia, sex hormone disturbances Diagnostic Evaluation - CBC: anemia - Elevated creatinine, BUN, phosphorus - Decreased Ca, HCO3 and CHONs (albumin) - ABG level: low blood pH, low pCO2 and HCO3 - 24-hour urine for creatinine, protein, creatinine clearance Nursing Interventions: GOAL: Conservation of renal function - Maintain F/E and acid base - Maintain Nutrition - Maintain Skin integrity - Detection of reversible cause and Rx - Treatment of anemia - Dialysis - Renal transplant DIET - Calories: high - Protein: restricted but increased in dialysis - Sodium: restricted to minimize Na and fluid retention - Potassium: restricted @ late stage - Calcium: increased d/t poor absorption r/t faulty vitamin D activation - Phosphorus: restricted d/t high blood levels r/t hypocalcemia - Saturated fat and cholesterol: restricted - Fluids: restricted.