Hyperglycemic Crisis in Acute Care

PURWOKO SUGENG H

GOALS
Understand the pathophysiology of Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Non-Ketotic Syndrome Identify appropriate treatment modalities for both Explain the principles of insulin administration via intravenous infusion

The Treatment Modalities for Optimal Glycemic Management Include:

Frequent blood glucose monitoring The administration of exogenous insulin Fluid and electrolyte replacement and maintenance Nutrition Hypoglycemia prevention
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The Treatment Modalities for Optimal Glycemic Management Include:

Careful administration and monitoring of concomitant pharmaceuticals Concurrent management of complications and co-morbidities

IN THE PRESENCE OF INSULIN, 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 used for tissue synthesis is stored as triglycerides in adipose cells

INSULIN DEFICIENCY
Liver cells release glycogen which converts to glucose Muscle cells release glycogen which converts to glucose Tissue breakdown releases amino acids which then release ketoacids and glucose Adipose cells release triglycerides which convert to free fatty acids and glycerol and thus, release glucose and ketone bodies

THE NORMAL METABOLISM OF GLUCOSE

Tissue Synthesis
Amino Acids (Proteins) Glycogen (carbohydrate storage) Liver Cells Glucose Adipose Cells Energy Triglyceride (fat storage) This is a simplified diagram of normal glucose metabolism when a sufficient quantity 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, the processes are reversed, yielding glucose from glycogen and fat for energy. Muscle Cells Glycogen (carbohydrate storage)

UNTREATED DIABETIC KETOACIDOSIS

Insulin Deficiency

Tissue Breakdown Amino Acids Ketoacids Glucose

Liver Cells Glycogen Glucose

Muscle Cells

Adipose Cells Triglyceride Free Fatty Acids and Glycerol Ketone Bodies (acetone, acetoacetic acid, B-hydroxybutyric acid)

Glucose Excess Glucose and Acid Formation Ketoacidosis

Pathofhysiology

DIABETIC KETOACIDOSIS
DKA is a serious, life-threatening event caused by a profound insulin deficiency. It is characterized by hyperglycemia, ketosis, dehydration and electrolyte imbalance.

LAB VALUES IN DKA

Blood glucose is > 250 mg/dl Urinary and serum ketones are positive Serum bicarbonate is < 18 mEq/L (Mild DKA could 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 slightly elevated Creatinine and BUN mildly increased WBCs increased Amylase increased Hgb and Hct increased LFTS 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 and terbutaline)

SIGNS & SYMPTOMS OF DKA

Nausea and vomiting Polydipsia, polyuria, and polyphagia Weakness Weight loss Anorexia Abdominal pain and cramping Visual disturbances Tachycardia

SIGNS & SYMPTOMS OF DKA

Hypotension Dehydration Warm, dry skin Rubor Kussmaul respirations Impaired consciousness and/or coma Fruity odor of ketones

TREATMENT OF DKA FLUID REPLACEMENT

IV fluid bolus of 0.9% NaCl at the rate of 1liter over 1 hour For hypovolemic shock, 0.9% NaCl at 1liter/hr For mild hypotension with sodium corrected high or normal, 0.45% NaCl, per protocol For mild hypotension with sodium corrected low, 0.9% NaCl Note: Potassium will be added to IV based on serum level When serum glucose reaches 200 mg/dL, change fluids to D50.45% NaCl

TREATMENT OF DKA INSULIN ADMINISTRATION

Regular insulin is the only IV insulin! Administer through a piggyback system into an existing IV line with an infusion pump Pre-flush the IV tubing with 50 ml. of the infusion to allow insulin to bind to the plastic macrotubing or 8.5 ml for microtubing 0.1 units/kg of weight is given IV bolus initially to adults to a maximum of 10 units. Hold insulin until Serum Potassium is > 3.3 mEq/L

INSULIN (CONT)
Step Two will be to initiate the insulin drip utilizing the Algorithms. Start with Algorithm 1. Move to higher algorithm if BG > 200 mg/dL and BG has not fallen by at least 50 mg/dl within the previous hour. Move to lower algorithm if BG < 150 mg/dl times 2 consecutive readings. When blood glucose falls below 200 mg /dl, the rate is typically decreased and the IV fluid is changed 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/bolus subcutaneous insulin protocol Subcutaneous basal insulin should be administered 2 hours before discontinuing the insulin drip If the patient will eat, subcutaneous prandial (rapid-acting insulin) should be administered during transition.

TREATMENT OF DKA POTASSIUM REPLACEMENT

Potassium is replaced based on plasma K+ concentrations Establish urine output to rule out renal failure If hypokalemic, K+ must be given immediately If not hypokalemic, 20-40 mEq/L must be given within the first 2-4 hours of treatment

POTASSIUM REPLACEMENT (CONT)

Administer K+ as K+Cl- or as potassium phosphate. DO NOT exceed 90 mEq/24 hr. of potassium phosphate because of danger of hypocalcemia. Monitor ECG. Hypokalemia causes a flattened T and the presence of U waves. Hyperkalemia causes peaked T waves , and if extremely high, a widened QRS complex.

POTASSIUM REPLACEMENT (CONT)

Administer K+ as K+Cl- or as potassium phosphate. DO NOT exceed 90 mEq/24 hr. of potassium phosphate because of danger of hypocalcemia. Monitor ECG. Hypokalemia causes a flattened T and the presence of U waves. Hyperkalemia causes peaked T waves , and if extremely high, a widened QRS complex.

POTASSIUM REPLACEMENT (CONT)

Recheck plasma K+ every two hours if plasma concentration of K+ is <4 or >6 mEq/L The goal of maintaining the plasma K+ is 3.5-5.0 mEq/L at all times

TREATMENT OF DKA BICARBONATE REPLACEMENT

Routine bicarbonate administration is not recommended if the pH is > 7.0 ! Sodium bicarbonate enhances hypokalemia

BICARBONATE ADMINISTRATION: BENEFITS

Correct extracellular acidosis Reduce excessive chloride administration Reduce respiratory rate and increase comfort Reduce cardiac irritability Increase responsiveness of vascular system to pressor agents

BICARBONATE ADMINISTRATION: POTENTIAL HAZARDS

Rapid reduction in plasma K+ Na+ overload in elderly persons or persons at risk for heart failure Exacerbate intracellular acidosis

TREATMENT OF DKA PHOSPHATE ADMINISTRATION

Phosphate concentration decreases with insulin therapy Calcium levels must be checked before administering phosphate Phosphate is replaced only at a level < 1.0 mg/dl Overzealous phosphate administration can cause severe hypocalcemia with no evidence of tetany

TREATMENT OF DKA COEXISTING INFECTION

Chest x-ray if warranted Appropriate cultures IV antibiotic therapy

TREATMENT OF DKA
Maintain airway Consider nasogastric tube if severe nausea and vomiting Observe for signs of cerebral edema, especially in children Auscultate lungs, assessing for heart failure Observe for signs/symptoms of hypoglycemia

PREVENTION OF DKA
Provide adequate patient and family education Make sure all items for self-care and diabetes management are available to the patient Provide follow-up medical care Effective communication with health care provider when ill

HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC SYNDROME

HHNS is a syndrome with four primary features including severe hyperglycemia, absence of ketosis, profound dehydration and 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 elderly individuals with Types 1 and 2 DM Illness such as infections, MI, GI bleeds, uremia and arterial thrombosis Stress Massive fluid loss from prolonged osmotic diuresis

CAUSES OF HHNS
Hypertonic feedings such as prolonged parenteral nutrition via IV infusion, highprotein or gastric tube feedings Pharmacologic agents such as thiazides, propranolol, phenytoin, steroids, flurosemide and chlorthalidone

SIGNS AND SYMPTOMS OF HHNS

Milder gastrointestinal symptoms Polydipsia and polyuria Weakness Anorexia Visual disturbances Tachycardia Hypotension Dehydration

SIGNS AND SYMPTOMS OF HHNS

Warm, dry skin Rubor Hyperpnea Weight loss Decreased mentation Focal neurological signs such as hemisensory deficits, hemiparesis, aphasia and seizures.

TREATMENT OF HHNS
The primary goal is rehydration! This is to restore circulating plasma volume and correct electrolyte imbalances IV fluid bolus of 0.9% NaCl at 1 liter/hour for initial fluid replacement. For hypovolemic shock, 0.9% NaCl at 1 liter/hr For mild hypotension with corrected high or normal 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 adults to 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 the Algorithms. Start with Algorithm 1. Move to higher algorithm if BG > 300 mg/dL and BG has not fallen by at least 50 mg/dl within the previous hour. Move to lower algorithm if BG < 250 mg/dl times 2 consecutive readings. When blood glucose falls below 250 mg /dl, the rate is typically decreased and the IV fluid is changed to a dextrose solution Blood glucose should drop 50-70 mg/dl/hr

Treatment of HHNS (cont)

Glucose hourly until stable while on an infusion Electrolyte levels should be monitored every 2-4 hours until stable Potassium and Phosphate are replaced as in DKA Treat any underlying medical conditions such as infection, especially urosepsis and pneumonia

PREVENTION OF HHNS
Provide patient, family and staff (such as nursing home) education and follow-up Keep fluids within reach or offer fluids every two hours to hospitalized or nursing home patients

Insulin Therapy
Continuous Intravenous Insulin Infusion if NPO, on Total Parenteral Nutrition, on Continuous Enteral Feeding Basal/Bolus insulin therapy in the fed state is accomplished by the administration of intermediate or long acting insulins and rapid and/or short acting insulins subcutaneously via Continuous Subcutaneous Insulin Infusion (ambulatory insulin pump) or multiple injections
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Evidence-Based Protocols
Continuous Intravenous Insulin Infusions Subcutaneous Insulin Management Continuous Subcutaneous Insulin Infusion Hypoglycemia

DKA
HHNS
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Continuous Intravenous Insulin Infusion Indications

Shock DKA HHNS Pregnancy Corticosteroid therapy Sepsis Transplantation Cardiopulmonary bypass surgery; perioperative management NPO, Continuous TPN, Continuous Enteral Feedings

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Intravenous Insulin
Fixed-rate insulin infusions Individualization of the rate of insulin infusion

Algorithms based on rate of change in blood glucose Neonatal, Pediatric (< 45 kg), Adult (> 45 kg)

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Continuous Intravenous Insulin Infusion Protocol

Initial IV Bolus-0.1 unit/kg to a maximum dose of 10 units Initiate algorithm 1 Move to a higher algorithm if BG > 200 mg/dl and BG has not fallen by at least 60 mg/dl within the previous hour. Move to a lower algorithm if BG < 80 mg/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/dL

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Predisposing Conditions
Renal insufficiency Malnutrition Hepatic disease/failure Sepsis Shock Pregnancy Malignant lesion Hyperkalemia (GIK cocktail) TPN Alcoholism and/or illegal drug use

Burns Gastroparesis or altered nutrient absorption Dementia CHF Stroke Altered ability to self-report Hypoglycemia Unawareness Aging Other metabolic disorders such as pituitary and adrenal insufficiency
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Triggers
Transportation off patient care unit NPO status, new/changed Interruption of IV dextrose therapy Interruption of TPN Interruption of enteral feedings Interruption of continuous venovenous hemodialysis Mental health/ECT Errors Schedules altered/timing

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Hypoglycemia Prevention
Hypoglycemia can cause harm! Thus, proper dosing of insulin, monitoring of blood glucose, appropriate nutrition, and evaluation of other pharmaceuticals is crucial to achieve and maintain glycemic control without causing harm from hypoglycemia.
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