Diabetes Management in Acute Care Settings: Insulin Therapy and Nutrition, Exams of Nutrition

Download Diabetes Management in Acute Care Settings: Insulin Therapy and Nutrition and more Exams Nutrition in PDF only on Docsity! Insulin in the inpatient setting and hyperglycemia. On admission to the hospital - Many, if not most, inpatients with hyperglycemia have a primary admission diagnosis únreľated diabetes Physician performs diagnostic work-up Perform an HbA1c for all patients with diabetes or hyperglycemia admitted to the hospital if not performed in the prior 3 months (Level B) Patients with diabetes should be on medical nutrition therapy with a balanced, hypocaloric, carbohydrate-consistent diet Involvement of a diabetes educator early in the course of admission will help particularly with newly diagnosed diabetic patients General principle Preferred therapy for inpatient management is always - INSULIN -ICU patients: Intravenous infusion with regular insulin - Floor patients: Subcutaneous basal-bolus regimen Non-insulin options - Non-insulin agents may be appropriate; however, only in patients who are clinically stable, in non- ICU settings, and who are expected to consume meals at regular intervals General disadvantages of non-insulin agents include: Relatively long half-life, delayed onset of action, and difficult to titrate In acute care settings we typically like drugs that are quick onset, short duration since they are easier to titrate Serious adverse effects uniquely problematic for inpatients Administration challenges given unpredictable meal patterns variable food absorption due to hemodynamic changes, and multiple factors influencing blood glucose levels Sulfonylurea - Glyburide Active metabolites! 50% renal excretion - Should NOT be recommended for use; problems particularly in the elderly and those with renal insufficiency Glipizide - Mostly inactive metabolites - 63-89% renal excretion (mostly inactive metabolites) Glimepiride - Has one weakly active metabolite via 2C9 pathway 60% renal excretion Watch renal function in ALL cases WHY? Sulfonylureas —> promote insulin secretion —>>subsequently eliminated kidneys Metformin facts inpatient - Risk of lactic acidosis in several types of inpatients Heart failure - Hypo-perfusion Older age Chronic pulmonary disease/hypoxic conditions Renal insufficiency Contraindicated if eGFR <30 mL/min Not recommended if eGFR 30 45 mL/min GI discomfort might make inpatient initiation difficult; low however, not entirely impossible provided that very starting dose is used IV contrast Discontinue metformin at the time of or before an IV contrast imaging procedure in patients with an eGFR 30 60 mL/min; in patients with a history of liver disease, alcoholism, or heart failure; or in patients who will be administered intra-arterial IV contrast. Re-evaluate eGFR 48 hours after the imaging procedure; re-start metformin if renal function is stable Thiazolidinediones inpatients - Edema is a common adverse event - major concern with inpatients that have heart failure, renal insufficiency, or volume overload Delayed onset of action makes utility for acute hyperglycemia very limited Start with correction Add basal if persistently hyperglycemic Add nutritional if patient is consuming regular meals Non-ICU (Type 1) - Admission hyperglycemia Start with correction basal need this to prevent DKA Add nutritional if patient is consuming regular meals Non-critically ill (non-ICU) patients - Subcutaneous basal-bolus insulin regimen with analogs is the preferred method of management Dosing - Calculated based on previous insulin daily dose - Weight based with starting dose of 0.2 0.6 units/kg/ day based on previous control. Total daily dose should be divided between basal and nutritional requirements (50-50%) - In naïve patients, need to start with a low dose and gradually titrate to effect - Often administered in the hospital after meals - Monitor blood glucose, serum creatinine, potassium RAPID ACTING ANALOGS ARE PREFERRED FOR - CORRECTION Regular Novolin R Humulin R Aspart Novolog Lispro Humalog Glulisine Apidra Correction insulin - Correction factor (CF) or insulin sensitivity factor refers to how much one unit of insulin will lower the blood glucose in mg/dL One way to estimate CF is 1700 or 1800 divided by total daily dose of insulin Correction dosing estimated using a formula (see next slide) (BG X)/Y # of units of correction to add to bolus dose "Sliding scales" is NOT the appropriate terminology for use because this denotes connotation of "passively" responding to high blood glucose, as opposed to proactively managing hyperglycemia The sole use of correction hot recommended! Completely fine to use for the first day or two. Remember, most patients have some other acute problem unrelated to their diabetes that is the reason for admission. Generally, we like to make progress in resolving that before aggressively managing their hyperglycemia assuming they are not in DKA/HHS Rapid acting analogs are preferred for use Correctional Insulin formula - (BG-150)/CF BG= finger stick BG taken prior to meal 150=bg goal for the inpatient. Hospitals will have protocols where the MD can pick the goal, X. CF = insulin sensitivity factor i.e. how much is 1 unit expected to drop the patient's BG? One way to calculate this is to take 1700 divided by total daily dose of insulin. Hospitals will have protocols where the MD can pick the insulin sensitivity or correction factor, Y. Example 10/17/17: 93 year old male admitted for chief complaint of abdominal pain. Past medical history significant for hypertension, Type 2 diabetes, GERD, and prostate cancer. CT confirms metastasis to the abdominal region. A BG check prior to bedtime around 9pm was 267 mg/dL and the patient has an active order for Novolog (aspart) correction before meals and at bedtime BP 121/52, HR = 73, K 4.2, Scr 1.1, WBC 11.7, Hb - 11.1 , estimated CrCl 37 Algorithm that was ordered was (BG - X)/Y with X 100, and Y 30 What's your evaluation? Patient received 6 units of Novolog for correction. Nurse checked Bg at 3:30am which was 133 mg/dL. What recommendations should be made during rounds? - X=100 is too aggressive Serum Creatinine is probably too high. Recommendation use a new algorithm Solid dots are SSI; open dots are basal bolus - Less wound infections, general complication s, ICU length of stay, and more hypoglycemia with the basal-bolus group vs. SSI Non-ICU patient (Type 2 or non- diabetic) with hyperglycemia: - Start with CORRECTION add BASAL add NUTRITIONAL Sole use of correction should be avoided except for first day or two Basal insulin type 1 - Onset of action: 1-2 hours Peak action: Theoretically, this is minimal, but probably will see some effect at 8-12 hours. Twice daily dosing is an option Duration: 6-23 hours Question: When do you check blood glucose? Basal insulin part II - Onset of action: 2-4 hours Peak action: Theoretically no peak, but may actually have a slight peak around 4 hours. Twice daily dosing is an option. With continuous feeding, the total daily nutritional component may be calculated as 1 unit of insulin for every 10 15 grams carbohydrate or 50 70% of total daily insulin administered every 6 hours (regular insulin) or 4 hours (analogs) For bolus feeds, give approximately 1 unit of insulin per 10 15 grams carbohydrate before each feeding For parenteral nutrition bags, regular insulin may be added to the bag particularly if >20 units of correction insulin was used in the past 24 hours (1 unit for every 10 grams of dextrose) Perioperative management - Target BG range should be 80 - 180 mg/dL Pre-operative assessment should be conducted for patients at high risk of ischemic heart disease, and those with autonomic neuropathy or renal insufficiency Withhold metformin on day of surgery Withhold any other oral hypoglycemic agents the morning of surgery or procedure Administer 60- 80% of long acting analog or pump basal insulin and give 2 usual NPřH dose Monitor blood glucose at least every 4 - 6 hours while NPO and dose with rapid acting analogs necessary Triggers for hypoglycemia - Sudden reduction in corticosteroid dose Reduced oral intake Emesis New NPO status Inappropriate timing of short-acting insulin relative to meals Reduced infusion rate of intravenous dextrose Unexpected interruption of oral, enteral, or parenteral feedings Altered ability of the patient to report symptoms Hypoglycemia Prevention and Treatment - Prevention is the key for inpatient settings! Active intervention strategies have been shown to significantly decrease the incidence of severe hypoglycemia Treatment is by nurse-initiated hypoglycemia treatment protocols Glucose 15-20 g Pure carbohydrate is preferred; fat and protein will delay absorption If SMBG 15 minute later shows continued hypoglycemia, repeat the treatment - Once POC (point of care) BG is normal, patient should consume meal or snack to prevent recurrent hypoglycemia - Glucagon 1 mg intramuscularly for severe hypoglycemia Background information for DKA - 168,000 hospitalizations for DKA in 2014 Components of DKA - Нурerglylcemia Acidosis Ketosis Components of HHS - Dehydration Hyperglycemia Hyperosmolarity DKA vs. HHS - DKA ->hyperglycemia » ketosis ketone body formation due to absolute insulin deficiency — >greater likelihood for the development of acidosis - Typical complication of Type 1 diabetes due to absolute insulin deficiency, but can arise in Type 2 patients as well called ketosis prone Type 2 diabetes HHS—-> more severe hyperglycemia » pronounced hyperosmolarity ->>typically more significant dehydration (vs. DKA) leading to acute kidney injury (pre-renal) - Typically seen in Type 2 patients who have a relative insulin deficiency Clinically they differ by the severity or degree of ketosis, metabolic acidosis, and dehydration DKA - Pathogenesis - Absolute Insulin Deficiency Which leads to increased Ketoacidosis Increase Counterregulatory Hormones Decrease Glucose utilization Increase Gluconcogenesis IncreasedGlycogenolysis Which leads to hyperglycemia Hyperglycemia HHS Pathogenesis - Increase in couterregulatory hormones with relative insulin deficiency Decreased glucose utilization Increased gluconeogenesis Increased glycogenolysis Which contribute to hyperglycemia. Anion gap Serum and urinary ketones - B-hydroxybutyric acid (stronger and generally more abundant) and acetoacetic acid - Direct measurement of B-hydroxybutyric acid is preferred for better gauge of ketosis Anion gap - (Na) (Cl HCO3) anion gap In DKA, anion gap is a result of the body using bicarbonate to neutralize excessive production of ketones General treatment algorithm for DKA/ HHS - IV Fluids —> restore circulatory volume and tissue perfusion IV Insulin —> correct hyperglycemia and acidosis Potassium (K) supplementation —> correct electrolyte imbalances Sodium bicarbonate —> extreme measure to correct acidosis V Fluids Severe Hypovolemia - Administer 0.9% Naci (1.0 Lhr) IV Fluids Mild dehydration Evaluate corrected serum Na Serum Na high or normal - 0.45% NaC (250-500 mihr) depending on hydration state When serum glucose reaches 200 mgld (DKA) or 300 mgid (HHS change to 5% dextrose with 0.45% NaCi at 150-250 mih IV Fluids Mild dehydration Evaluate corrected serum Na Serum Na low - S60 ORN (250-500 mihr) depending on hydration state When serum glucose reaches 200 mgld (DKA) or 300 mgid (HHS change to 5% dextrose with 0.45% NaCi at 150-250 mih IV Fluids - Typically given as NS (normal saline) in either the 0.9% or 0.45% concentration Goals - Expand circulatory volume and tissue perfusion (improved kidney perfusion demonstrated by serum creatinine) Monitoring - BP - Serum electrolytes Serum creatinine, BUN, urine output Add D5W (dextrose 5%) to the solution when BG <200 300 mg/dL Why do this if they just had a hyperglycemic episode? Insulin in DKA/HHS - Given most commonly as an intravenous (IV) regular insulin infusion - Studies have shown that SQ Novolog and Humalog also effective although typically IV regular insulin is what is preferred in practice Goals PRIMARY GOAL in DKA shut off lipolysis Normal pH and HC03 For both DKA and HHSlower blood glucose Monitoring pH, HCO3 BG (typically want to lower this 50 75 mg/dL per hour) Why do you keep BG 150 200 mg/dL (DKA) or 200 300 mg/dL (HHS) until resolution of symptoms? Transition to subcutaneous insulin once patient is out of the acute hyperglycemic stage (give subcutaneous insulin 1 2 hours before túrning off IV insulin) Insulin vs. potassium - Acidosis—> K moves out (extracellular shift)-> serum K is then artificially elevated Treatment with insulin —> resolution of acidosis K moves back in Serum K dropping low —> Cardiac arrhythmia! Potassium in DKA/HHS - Changes in serum potassium levels are due to intracellular and extracellular shifting of potassium due to changes in acidosis (pH) over the course of therapy Goal - Normalize serum potassium and prevent cardiac arrhythmias Monitoring: Potassium supplementation If serum K is below the normal range Yes If serum K is in the normal range YES - If serum K is above the normal range NO In addition, HOLD INSULIN if serum K is <3.3 mEq/L - Why? Bicarbonate - Correct severe acidosis (weak evidence). Generally NOT recommended. Resolution TREATMENT CONTINUES UNTIL RESOLUTION - DKA - BG <200 mg/dL -Two the following: HCO3 15 mEq/L venous pH >7.30 anion gap s12 mEq/L HHS - BG <200 mg/dL - Normal osmolality - Normal mental status Prevention - Address barriers to adherence - Educate on appropriate, compliant use of insulin and other anti- diabetic agents