| Term 
 
        | decompensation of diabetes higher stress due to illnesses (infections, fever, trauma, or other medical stresses)
 decreased physical activities in the hospital
 withholding of diabetic treatments
 administration of IV dextrose, parenteral or enteral nutrition
 administration of pharmacologic agents (glucocorticoids, vasopressors, fluroquinolones)
 |  | Definition 
 
        | causes of inpatient hyperglycemia |  | 
        |  | 
        
        | Term 
 
        | suppressed immune system impaired vascular responses
 hyperreactive platelets and coagulation
 inflammation
 increased oxidative stress
 |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | difficult to achieve very tight glucose target (80-110 mg/dL) higher rates of hypoglycemia were reported
 NICE-SUGAR (2009):  largest study to date in critically ill patients (medical and surgical ICU), increased 90 day mortality in intensive group, more severe hypoglycemia
 meta-analysis (2009):  no overall mortality benefit with intensive glycemic control, decreased mortality in surgical ICU patients only, 6-fold increase in severe hypoglycemia (<40 mg/dL)
 |  | Definition 
 
        | recent studies on the effect of tight glycemic control for hospitalized patients |  | 
        |  | 
        
        | Term 
 
        | has not been consistently shown to decrease mortality in critically ill patients may actually increase mortality
 leads to increased risk of hypoglycemia
 |  | Definition 
 
        | why is a glycemic goal of 80-100 mg/dL not appropriate? |  | 
        |  | 
        
        | Term 
 
        | ICU:  140-180 mg/dL non-ICU:  preprandial = < 140 mg/dL; random = < 180 mg/dL
 clinically stable patients with previously successful tight glycemic control may have lower glycemic goals during the hospitalization
 terminally ill patients or patients with severe comorbidities may have higher glycemic goals
 no randomized controlled trials have been done in hospitalized patients outside of ICU setting
 |  | Definition 
 
        | glycemic goals in hospitalized patients |  | 
        |  | 
        
        | Term 
 
        | hyperglycemia:  DM is typically not the primary medical problem, frequent interruptions in glucose lowering medications, nursing shortage, skepticism about the effect of good glycemic control, fear of hypoglycemia, lack of protocols/algorithms hypoglycemia:  altered nutrition status (NPO, reduced oral intake, interruption in nutritional support, emesis), organ failures (renal disease), sudden reduction in corticosteroid dose, altered ability of patients to self-report symptoms
 lack of protocols/algorithms
 |  | Definition 
 
        | barriers to optimal glycemic control in hospitalized patients:  causes of hyper and hypoglycemia |  | 
        |  | 
        
        | Term 
 
        | measure blood glucose at hospital admission in all patients identify ("flag") patients with PMH of DM
 measure A1C at hospital admission if:  hyperglycemia is present and no PMH of DM or PMH of DM and no A1C within previous 3 months
 plasma glucose monitoring:  in all patients with PMH of DM, hyperglycemia at admission, or at high risk for hyperglycemia; typical frequency is QID corresponding with each meal and HS; if patient NPO or receiving continuous nutrition support q4-6h is sufficient; frequency may be increased in severe illness
 individualized diets in patients with PMH of DM:  consistent CHO diet, may use CHO counting to determine prandial insulin doses
 individualized DM therapy:  guidelines currently recommend insulin in most hospitalized patients; may use non-insulin agents in selected patients (clinically stable, expected to consume meals at regular intervals, no newly developed contraindications)
 |  | Definition 
 
        | general approach to management of inpatient hyperglycemia |  | 
        |  | 
        
        | Term 
 
        | SFUs - hypoglycemia (especially in people with poor oral intake), long duration of action glinides - do not have clinical data for inpatient use, mainly used for post-prandial hyperglycemia so not ideal for NPO or patients with poor oral intake
 metformin - GI ADRs may be problematic, increased risk of lactic acidosis due to various conditions (decompensated HF, hypoperfusion, renal insufficiency, respiratory distress/failure, need for contrast in imaging tests)
 TZDs - delayed onset of action, increased intravascular volume
 a-glucosidase inhibitors - mainly reduce post-prandial hyperglycemia, high incidence of GI ADRs
 pramlintide/exenatide - mainly reduce postprandial hyperglycemia, nausea is the most common ADR
 DPP4 inhibitors - limited experience and no inpatient data
 |  | Definition 
 
        | limitations of non-insulin agents:  SFUs, glinides, metformin, TZDs, a-glucosidase inhibitors, pramlintide/exenatide, DPP4 inhibitors |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | (subcutaneous/IV) insulin is the preferred route in non-critically ill patients |  | 
        |  | 
        
        | Term 
 
        | basal insulin provides coverage for basic metabolic function:  if patient NPO they may not need exogenous basal insulin if patient has enough endogenous insulin synthesis, patients with insulin deficiency (T1DM) still need basal insulin even if NPO or have limited oral intake in order to prevent ketoacidosis nutritional insulin provides coverage for meals and/or other nutritional support (TPN, enteral feedings, dextrose infusion, nutritional supplement)
 |  | Definition 
 
        | what is the difference between basal and nutritional insulin? |  | 
        |  | 
        
        | Term 
 
        | need to review insulin regimen at least daily reassess regimen if insulin not at goal or if any BG < 100 mg/dL
 modify regimen if any BG < 70 mg/dL
 |  | Definition 
 
        | how often should an insulin regimen be reviewed for a patient in a hospital? |  | 
        |  | 
        
        | Term 
 
        | supplemental/correctional insulin |  | Definition 
 
        | refers to additional insulin injections between scheduled doses to correct for unexpected hyperglycemia, usually dosed based on patient's blood glucose level |  | 
        |  | 
        
        | Term 
 
        | regular insulin:  inexpensive, longer duration may be problematic rapid-acting insulin:  ideal preparation for isolated hyperglycemia without affecting subsequent glucose readings, expensive
 |  | Definition 
 
        | comparison of the types of insulin used for supplemental/correctional insulin |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | usually refers to the use of regular insulin dosed based on BG without any scheduled insulin ineffective for hyperglycemia when used as monotherapy
 gives no incentive to adjust scheduled therapy
 usually not individualized dosing
 reactive approach rather than proactive
 often leads to fluctuation in BG levels
 |  | 
        |  | 
        
        | Term 
 
        | continuous IV infusion uses regular insulin
 |  | Definition 
 
        | (subcutaneous/continuous IV infusion) is the preferred route for ICU patients |  | 
        |  | 
        
        | Term 
 
        | advantages:  most effective in achieving pre-specified BG levels, allows rapid dosing adjustment, has been shown to decrease mortality and morbidity in some studies disadvantages:  very labor intensive (requires q1-2h glucose monitoring), increases risk of hypoglycemia
 |  | Definition 
 
        | advantages and disadvantages to IV insulin infusions |  | 
        |  | 
        
        | Term 
 
        | CRITICAL ILLNESS HYPERGLYCEMIC CRISIS
 preoperative, intraoperative, and postoperative care
 post heart surgery
 post organ transplant
 cardiogenic shock
 high dose glucocorticoid therapy
 prolonged NPO in T1DM
 |  | Definition 
 
        | indications of IV insulin infusions |  | 
        |  | 
        
        | Term 
 
        | first dose of SC insulin should be given before IV insulin is discontinued if intermediate or long acting insulin is used alone, administer 2-3 hours prior
 if combination of basal and preprandial insulin, basal insulin can be initiated at any time of the day
 administer short or rapid acting insulin 1-2 hours prior to discontinuing IV infusion
 |  | Definition 
 
        | transition from CIII to SC |  | 
        |  | 
        
        | Term 
 
        | increased insulin sensitivity:  T1DM, elderly decreased insulin clearance:  renal failure patients, patients with organ failure, liver disease
 diminished glycogen stores:  malnourished patients
 |  | Definition 
 
        | in what patients would you use less aggressive insulin dosing? |  | 
        |  | 
        
        | Term 
 
        | hyperglycemia in patients with prior DM:  if A1C is elevated at admission, preadmission regimens need to be revised hyperglycemic patients without prior DM (A1C should be used to differentiate between stress hyperglycemia and undiagnosed DM):  patients with newly diagnosed DM should receive appropriate education and follow up, patients with stress hyperglycemia still need appropriate follow up with a physician
 |  | Definition 
 
        | follow up upon discharge from the hospital |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | a medical emergency in which severe lack of insulin results in the breakdown of body fat for energy, which leads to accumulation of ketones in the body |  | 
        |  | 
        
        | Term 
 
        | hyperosmolar hyperglycemic state |  | Definition 
 
        | a medical emergency in which extremely high serum glucose level results in increased urination, which leads to severe dehydration and impaired renal function |  | 
        |  | 
        
        | Term 
 
        | causes:  absolute deficiency in insulin OR insufficient insulin coupled with increased counterregulatory stress hormones hyperglycemia -> glucosuria -> osmotic diuresis -> dehydration and loss of Na and K
 increased lipolysis -> increased FFA -> increased ketone bodies -> increased ketonemia and metabolic acidosis
 evolves over a short period of time (< 24 hours)
 |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | causes:  insufficient insulin AND insulin resistant residual insulin is sufficient enough to inhibit lipolysis therefore minimizing ketosis, but not hyperglycemia
 hyperglycemia -> glucosuria -> osmotic diuresis -> severe dehydration (hyperosmolality), loss of electrolytes, and impaired renal function
 reduction in urinary excretion of glucose leads to more severe hyperglycemia than in DKA
 evolves over days and weeks
 |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | hyperglycemia (HHS>DKA) dehydration (HHS>DKA)
 Na and K are the main electrolytes affected
 sodium: decreased Na and water reabsorption and increased urinary Na loss lead to net loss of total body Na (need to calculate a corrected Na based on glucose level before accessing total Na deficit)
 potassium:  dehydration and acidosis (in DKA) cause shifting of K out of cells, insulinopenia leads to impaired K entry into cells, increased K in ECF leads to increased urinary loss
 serum Na and K concentrations depend on degree of dehydration
 other electrolytes effected include:  Cl, Phos, Ca, Mg
 metabolic acidosis = DKA
 hyperosmolality = HHS
 |  | Definition 
 
        | major components of DKA and HHS (hyperglycemia, dehydration, Na, K, pH, osmolality) |  | 
        |  | 
        
        | Term 
 
        | INFECTION (PNEUMONIA, UTI, SEPSIS) inappropriate insulin therapy (omission, inadequate dose, or insulin pump problems)
 new onset of DM
 CVD
 pregnancy
 trauma
 hyperthyroidism
 pancreatitis
 drugs
 |  | Definition 
 
        | precipitating factors for DKA and HHS |  | 
        |  | 
        
        | Term 
 
        | symptoms:  history of polyuria, polydipsia, and weight loss; N/V, abdominal pain; fruity odorous breath (DKA); weakness and muscle cramps; altered mental status (drowsy, stupor, coma, hemiparesis, hemianopsia, and seizure) signs:  dehydration (signs and symptoms include dry mucous membranes, reduced skin turgor, sunken eyes, altered mental status, weight loss, hypotension, tachycardia, prolonged capillary refill and even shock); hyperventilation, coma (more frequent in HHS)
 |  | Definition 
 
        | clinical presentation of DKA or HHS |  | 
        |  | 
        
        | Term 
 
        | plasma glucose:  > 250 mg/dL serum Na:  low
 serum K:  low-high
 ARTERIAL PH:  < 7.3
 SERUM BICARB:  10-18
 URINE KETONES:  PRESENT
 SERUM KETONES:  PRESENT
 serum osmolality:  variable
 ANION GAP:  > 10-12
 |  | Definition 
 
        | diagnosis of DKA based on lab levels |  | 
        |  | 
        
        | Term 
 
        | PLASMA GLUCOSE:  > 600 mg/dL serum Na:  normal or increased
 serum K:  low - high
 arterial pH:  > 7.3
 serum bicarb:  > 18
 urine ketones:  small
 serum ketones:  small
 SERUM OSMOLALITY:  > 320 (normal 275-290)
 anion gap:  variable
 |  | Definition 
 
        | diagnosis of HHS based on lab values |  | 
        |  | 
        
        | Term 
 
        | risk of mortality increases in very young or very old negative prognosis factors:  hypotension, hypothermia, coma
 |  | Definition 
 
        | negative prognosis factors for DKA and HHS |  | 
        |  | 
        
        | Term 
 
        | correction of hyperglycemia correction of dehydration
 correction of electrolytes (sodium and potassium)
 correction of metabolic acidosis in DKA
 treatment of underlying cause
 |  | Definition 
 
        | general approach to treatment of DKA or HHS |  | 
        |  | 
        
        | Term 
 
        | continuous IV insulin infusion: if plasma glucose does not fall by 50-75 mg/dL in the 1st hour, increase infusion rate every hour until steady decline is reached
 maintenance insulin infusion when plasma glucose reaches 200 mg/dL in DKA or 300 mg/dL in HHS
 once plasma glucose is at 200 (DKA) or 300 (HHS) then decrease insulin drip and add dextrose to IV fluids
 adjust infusion rate and dextrose amount to maintain 150-200 mg/dL until acidosis resolves (DKA) or 250-300 mg/dL until hyperosmolality resolves and mental status improves (HHS)
 intermittent SC rapid-acting insulin may be used in mild DKA:
 bolus dose and q1-2h injections to achieve glucose around 250 mg/dL
 then dose adjust until DKA resolves
 no differences in efficacy compared to IV insulin in mild DKA
 allows treatment on general medicine floor or ED which cuts costs
 MUST HOLD INSULIN IF K < 3.3 MEQ/L!!!
 |  | Definition 
 
        | correction of hyperglycemia in DKA and HHS |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | at what K level must insulin be held? |  | 
        |  | 
        
        | Term 
 
        | need repletion of both intravascular and estravascular volume 0.9% NaCl (normal saline) should be infused
 subsequent fluid depends on serum Na concentrations:  normal or elevated Na - 0.45% NaCl; low Na - 0.9% NaCl
 when plasma glucose reaches 200 mg/dL in DKA or 300 mg/dL in HHS, switch to D5W in 1/2NS
 infusion rate must be adjusted for cardiac and renal dysfunction
 monitor BP and I/O to better assess fluid status
 |  | Definition 
 
        | correction of dehydration in DKA and HHS |  | 
        |  | 
        
        | Term 
 
        | sodium:  replaced adequately with fluid replacement potassium:
 usually depleted due to urinary loss but serum concentration may be low, normal, or high
 replacement dose depends on serum K level
 low (<3.3):  treatment immediately with K and HOLD INSULIN THERAPY until K > 3.3
 normal (>3.3 but <5.2): give supplemental K in IV fluids while patient is on IV insulin
 high (>5.2):  no replacement until level drops (usually 1-2 hours after treatment) and recheck q2h
 must consider renal function
 goal K level = 4-5 mEq/L
 |  | Definition 
 
        | correction of electrolytes (Na and K) in DKA and HHS |  | 
        |  | 
        
        | Term 
 
        | acidosis will correct with insulin therapy sodium bicarbonate may be necessary only in SEVERE acidosis
 pH < 6.9:  bicarb should be given until pH > 7
 pH >/= 6.9:  no bicarb needed
 need to monitor K and replace accordingly
 |  | Definition 
 
        | correction of metabolic acidosis in DKA |  | 
        |  | 
        
        | Term 
 
        | SC insulin may be initated when blood glucose < 200 mg/dL and DKA resolves (serum bicarbonate >/= 15 mEq/L, pH > 7.3, and anion gap = 12 mEq/L) or HHS resolves (osmolality and metal status normalizes) SC insulin should provide basal and prandial coverage
 first dose of SC insulin should be given before IV insulin is discontinued, depending on type of SC insulin:  if intermediate or long acting insulin used alone, administer 2-3 hours prior to discontinuation of IV insulin; administer short or rapid acting insulin 1-2 hours prior to discontinuing IV infusion
 |  | Definition 
 
        | transition from IV insulin to SC for DKA and HHS |  | 
        |  |