• Save
Hyperglycemic crisis ppt.
Upcoming SlideShare
Loading in...5
×
 

Hyperglycemic crisis ppt.

on

  • 1,404 views

 

Statistics

Views

Total Views
1,404
Views on SlideShare
1,404
Embed Views
0

Actions

Likes
1
Downloads
0
Comments
0

0 Embeds 0

No embeds

Accessibility

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    Hyperglycemic crisis ppt. Hyperglycemic crisis ppt. Presentation Transcript

    • Hyperglycemic Crisis in AcuteCareFairview Health Services2007Carol Manchester, MSN, APRN, BC-ADM,CDEDiabetes Clinical Nurse SpecialistUniversity of Minnesota Medical Center,FairviewUniversity of Minnesota Children’s Hospital,Fairview
    • GOALS• Understand the pathophysiology ofDiabetic Ketoacidosis and HyperosmolarHyperglycemic Non-Ketotic Syndrome• Identify appropriate treatment modalitiesfor both• Explain the principles of insulinadministration via intravenous infusion
    • The Treatment Modalities forOptimal Glycemic ManagementInclude:• Frequent blood glucose monitoring• The administration of exogenous insulin• Fluid and electrolyte replacement andmaintenance• Nutrition• Hypoglycemia prevention 3
    • The Treatment Modalities forOptimal Glycemic ManagementInclude:• Careful administration and monitoring ofconcomitant pharmaceuticals• Concurrent management of complicationsand co-morbidities4
    • IN THE PRESENCE OFINSULIN, GLUCOSE:• is used as energy by the muscle cells• is stored as glycogen in the muscle cells• is stored as glycogen in the liver• enables amino acids/proteins to be usedfor tissue synthesis• is stored as triglycerides in adipose cells
    • INSULIN DEFICIENCY• Liver cells release glycogen which converts toglucose• Muscle cells release glycogen which converts toglucose• Tissue breakdown releases amino acids whichthen release ketoacids and glucose• Adipose cells release triglycerides which convertto free fatty acids and glycerol and thus, releaseglucose and ketone bodies
    • THE NORMAL METABOLISMOF GLUCOSEEnergyAdipose CellsGlucose Muscle CellsGlycogen(carbohydratestorage)Amino Acids(Proteins)Tissue SynthesisTriglyceride (fat storage)Liver CellsGlycogen(carbohydratestorage)This is a simplified diagram of normal glucose metabolism when a sufficientquantity of insulin exists within the body and there are no receptor defects present.When the plasma glucose levels become too low in the normal state, theprocesses are reversed, yielding glucose from glycogen and fat for energy.
    • UNTREATED DIABETICKETOACIDOSISGlucoseKetoacidsAmino AcidsTissue BreakdownKetoacidosisExcess Glucoseand Acid FormationGlucoseGlycogenLiver Cells Muscle CellsGlucoseKetone Bodies(acetone,acetoacetic acid,B-hydroxybutyric acid)Free Fatty Acidsand GlycerolTriglycerideAdipose CellsInsulin Deficiency
    • DIABETIC KETOACIDOSIS• DKA is a serious, life-threateningevent caused by a profound insulindeficiency. It is characterized byhyperglycemia, ketosis,dehydration and electrolyteimbalance.
    • LAB VALUES IN DKA• Blood glucose is > 250 mg/dl• Urinary and serum ketones are positive• Serum bicarbonate is < 18 mEq/L (Mild DKAcould be 15- 18)• Arterial pH is < 7.3• Anion gap is > 10 mEq/L• Potassium is low, normal or high
    • LAB VALUES IN DKA• Phosphate usually normal or slightlyelevated• Creatinine and BUN mildly increased• WBC’s increased• Amylase increased• Hgb and Hct increased• LFT’S can be elevated
    • CAUSES OF DKA• New onset of Type 1 DM• Illness/Infection• Stress• Omission of insulin• Mismanagement of sick days• Pregnancy• Insulin pump malfunction• Drugs-Corticosteroids, Thiazides,sympathomimetic agents (Dobutamine andterbutaline)
    • SIGNS & SYMPTOMSOF DKA• Nausea and vomiting• Polydipsia, polyuria, and polyphagia• Weakness• Weight loss• Anorexia• Abdominal pain and cramping• Visual disturbances• Tachycardia
    • SIGNS & SYMPTOMSOF DKA• Hypotension• Dehydration• Warm, dry skin• Rubor• Kussmaul respirations• Impaired consciousness and/or coma• Fruity odor of ketones
    • TREATMENT OF DKAFLUID REPLACEMENT• IV fluid bolus of 0.9% NaCl at the rate of 1literover 1 hour• For hypovolemic shock, 0.9% NaCl at 1liter/hr• For mild hypotension with sodium corrected highor normal, 0.45% NaCl, per protocol• For mild hypotension with sodium corrected low,0.9% NaCl• Note: Potassium will be added to IV based onserum level• When serum glucose reaches 200 mg/dL,change fluids to D50.45% NaCl
    • TREATMENT OF DKAINSULIN ADMINISTRATION• Regular insulin is the only IV insulin!• Administer through a piggyback system into anexisting IV line with an infusion pump• Pre-flush the IV tubing with 50 ml. of theinfusion to allow insulin to bind to the plasticmacrotubing or 8.5 ml for microtubing• 0.1 units/kg of weight is given IV bolus initially toadults to a maximum of 10 units.• Hold insulin until Serum Potassium is > 3.3mEq/L
    • INSULIN (CONT)• Step Two will be to initiate the insulin driputilizing the Algorithms. Start with Algorithm 1.• Move to higher algorithm if BG > 200 mg/dL andBG has not fallen by at least 50 mg/dl within theprevious hour.• Move to lower algorithm if BG < 150 mg/dl times2 consecutive readings.• When blood glucose falls below 200 mg /dl, therate is typically decreased and the IV fluid ischanged to a dextrose solution• Blood glucose should drop 50-70 mg/dl/hr
    • INSULIN (CONT)• Hourly blood glucoses are necessary• Transition from IV insulin to basal/bolussubcutaneous insulin protocol• Subcutaneous basal insulin should beadministered 2 hours before discontinuingthe insulin drip• If the patient will eat, subcutaneousprandial (rapid-acting insulin) should beadministered during transition.
    • TREATMENT OF DKAPOTASSIUM REPLACEMENT• Potassium is replaced based on plasmaK+ concentrations• Establish urine output to rule out renalfailure• If hypokalemic, K+ must be givenimmediately• If not hypokalemic, 20-40 mEq/L must begiven within the first 2-4 hours of treatment
    • POTASSIUM REPLACEMENT(CONT)• Administer K+ as K+Cl- or as potassiumphosphate. DO NOT exceed 90 mEq/24hr. of potassium phosphate because ofdanger of hypocalcemia.• Monitor ECG. Hypokalemia causes aflattened T and the presence of U waves.Hyperkalemia causes peaked T waves ,and if extremely high, a widened QRScomplex.
    • POTASSIUM REPLACEMENT(CONT)• Administer K+ as K+Cl- or as potassiumphosphate. DO NOT exceed 90 mEq/24hr. of potassium phosphate because ofdanger of hypocalcemia.• Monitor ECG. Hypokalemia causes aflattened T and the presence of U waves.Hyperkalemia causes peaked T waves ,and if extremely high, a widened QRScomplex.
    • POTASSIUM REPLACEMENT(CONT)• Recheck plasma K+ every two hours ifplasma concentration of K+ is <4 or >6mEq/L• The goal of maintaining the plasma K+ is3.5-5.0 mEq/L at all times
    • TREATMENT OF DKABICARBONATEREPLACEMENT• Routine bicarbonate administration is notrecommended if the pH is > 7.0 !• Sodium bicarbonate enhanceshypokalemia
    • BICARBONATEADMINISTRATION: BENEFITS• Correct extracellular acidosis• Reduce excessive chlorideadministration• Reduce respiratory rate and increasecomfort• Reduce cardiac irritability• Increase responsiveness of vascularsystem to pressor agents
    • BICARBONATEADMINISTRATION:POTENTIAL HAZARDS• Rapid reduction in plasma K+• Na+ overload in elderly persons orpersons at risk for heart failure• Exacerbate intracellular acidosis
    • TREATMENT OF DKAPHOSPHATEADMINISTRATION• Phosphate concentration decreases withinsulin therapy• Calcium levels must be checked beforeadministering phosphate• Phosphate is replaced only at a level < 1.0mg/dl• Overzealous phosphate administration cancause severe hypocalcemia with no evidenceof tetany
    • TREATMENT OF DKACOEXISTING INFECTION• Chest x-ray if warranted• Appropriate cultures• IV antibiotic therapy
    • TREATMENT OF DKA• Maintain airway• Consider nasogastric tube if severenausea and vomiting• Observe for signs of cerebral edema,especially in children• Auscultate lungs, assessing for heartfailure• Observe for signs/symptoms ofhypoglycemia
    • PREVENTION OF DKA• Provide adequate patient and familyeducation• Make sure all items for self-care anddiabetes management are available to thepatient• Provide follow-up medical care• Effective communication with health careprovider when ill
    • HYPEROSMOLARHYPERGLYCEMIC NON-KETOTIC SYNDROME• HHNS is a syndrome with four primaryfeatures including severe hyperglycemia,absence of ketosis, profound dehydrationand neurologic manifestations
    • LAB VALUES IN HHNS• Usually > 600 mg/dl• Na+ normal or high• K+ is high, normal or low• Serum Bicarbonate is >15mEq/L• Arterial pH is >7.3• Serum osmolality is high; >320 mmol/kg• Minimal ketonuria or ketonemia
    • CAUSES OF HHNS• Age; HHNS is more common in elderlyindividuals with Types 1 and 2 DM• Illness such as infections, MI, GI bleeds,uremia and arterial thrombosis• Stress• Massive fluid loss from prolonged osmoticdiuresis
    • CAUSES OF HHNS• Hypertonic feedings such as prolongedparenteral nutrition via IV infusion, high-protein or gastric tube feedings• Pharmacologic agents such as thiazides,propranolol, phenytoin, steroids,flurosemide and chlorthalidone
    • SIGNS AND SYMPTOMSOF HHNS• Milder gastrointestinal symptoms• Polydipsia and polyuria• Weakness• Anorexia• Visual disturbances• Tachycardia• Hypotension• Dehydration
    • SIGNS AND SYMPTOMSOF HHNS• Warm, dry skin• Rubor• Hyperpnea• Weight loss• Decreased mentation• Focal neurological signs such ashemisensory deficits, hemiparesis,aphasia and seizures.
    • TREATMENT OF HHNS• The primary goal is rehydration! This is torestore circulating plasma volume and correctelectrolyte imbalances• IV fluid bolus of 0.9% NaCl at 1 liter/hour forinitial fluid replacement.• For hypovolemic shock, 0.9% NaCl at 1 liter/hr• For mild hypotension with corrected high ornormal sodium, 0.45% NaCl• For mild hypotension with corrected low sodium,0.9% NaCl• When serum glucose reaches 250 mg/dl,change to D5 with .45% NaCl• Potassium is added based on serum level
    • TREATMENT OF HHNS(CONT)• 0.1 units/kg of weight is given IV bolus initially to adultsto a maximum of 10 units.• Hold insulin until Serum Potassium is > 3.3 mEq/L• Step Two will be to initiate the insulin drip utilizing theAlgorithms. Start with Algorithm 1.• Move to higher algorithm if BG > 300 mg/dL and BG hasnot fallen by at least 50 mg/dl within the previous hour.• Move to lower algorithm if BG < 250 mg/dl times 2consecutive readings.• When blood glucose falls below 250 mg /dl, the rate istypically decreased and the IV fluid is changed to adextrose solution• Blood glucose should drop 50-70 mg/dl/hr
    • Treatment of HHNS (cont)• Glucose hourly until stable while on aninfusion• Electrolyte levels should be monitoredevery 2-4 hours until stable• Potassium and Phosphate are replaced asin DKA• Treat any underlying medical conditionssuch as infection, especially urosepsisand pneumonia
    • PREVENTION OF HHNS• Provide patient, family and staff (such asnursing home) education and follow-up• Keep fluids within reach or offer fluidsevery two hours to hospitalized or nursinghome patients
    • Insulin Therapy• Continuous Intravenous Insulin Infusion ifNPO, on Total Parenteral Nutrition, onContinuous Enteral Feeding• Basal/Bolus insulin therapy in the fed stateis accomplished by the administration ofintermediate or long acting insulins andrapid and/or short acting insulinssubcutaneously via ContinuousSubcutaneous Insulin Infusion(ambulatory insulin pump) or multipleinjections 40
    • Evidence-Based Protocols• Continuous Intravenous Insulin Infusions• Subcutaneous Insulin Management• Continuous Subcutaneous Insulin Infusion• Hypoglycemia• DKA• HHNS41
    • Continuous IntravenousInsulin Infusion Indications• Shock• DKA• HHNS• Pregnancy• Corticosteroid therapy• Sepsis• Transplantation• Cardiopulmonary bypass surgery;perioperative management• NPO, Continuous TPN, Continuous EnteralFeedings 42
    • Intravenous Insulin• Fixed-rate insulin infusions• Individualization of the rate of insulin infusion• Algorithms based on rate of change in bloodglucose• Neonatal, Pediatric (< 45 kg), Adult (> 45 kg)43
    • Continuous Intravenous InsulinInfusion Protocol• Initial IV Bolus-0.1 unit/kg to a maximumdose of 10 units• Initiate algorithm 1• Move to a higher algorithm if BG > 200mg/dl and BG has not fallen by at least 60mg/dl within the previous hour.• Move to a lower algorithm if BG < 80mg/dl X 2 consecutive readings.• Transition as with DKA and HHNS.
    • Classifications of Hypoglycemia• Severe hypoglycemia; < 45 mg/dL• Moderate hypoglycemia; 45-59 mg/dL• Mild hypoglycemia; 60-70 mg/dL45
    • Predisposing Conditions• Renal insufficiency• Malnutrition• Hepatic disease/failure• Sepsis• Shock• Pregnancy• Malignant lesion• Hyperkalemia (GIKcocktail)• TPN• Alcoholism and/or illegaldrug use• Burns• Gastroparesis or alterednutrient absorption• Dementia• CHF• Stroke• Altered ability to self-report• HypoglycemiaUnawareness• Aging• Other metabolic disorderssuch as pituitary andadrenal insufficiency46
    • Triggers• Transportation offpatient care unit• NPO status,new/changed• Interruption of IVdextrose therapy• Interruption of TPN• Interruption of enteralfeedings• Interruption ofcontinuousvenovenoushemodialysis• Mental health/ECT• Errors• Schedulesaltered/timing47
    • Hypoglycemia Prevention• Hypoglycemia can cause harm!• Thus, proper dosing of insulin, monitoringof blood glucose, appropriate nutrition,and evaluation of other pharmaceuticals iscrucial to achieve and maintain glycemiccontrol without causing harm fromhypoglycemia.48
    • Concomitant Pharmaceuticals• Polypharmacy/reconciliation• Herbals• Agents that lower blood glucose– Pharmagrams for fluorquinolones, octreotide• Agents that raise blood glucose such asglucocorticoids– Steroid taper then insulin taper?– Alternative choices– Timing of dosages– Piggyback diluents49
    • Comorbid Conditions• Pneumonia, urinary tract infection,sinusitus, congestive heart failure,etc.must be identified and treated.• Diabetes is usually the comorbid condition50