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

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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

Energy

Adipose Cells

Glucose Muscle CellsGlycogen

(carbohydratestorage)

Amino Acids(Proteins)

Tissue Synthesis

Triglyceride (fat storage)

Liver CellsGlycogen

(carbohydratestorage)

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.

UNTREATED DIABETIC KETOACIDOSIS

Glucose

Ketoacids

Amino Acids

Tissue Breakdown

Ketoacidosis

Excess Glucoseand Acid Formation

Glucose

Glycogen

Liver Cells Muscle Cells

Glucose

Ketone Bodies (acetone,

acetoacetic acid, B-hydroxybutyric acid)

Free Fatty Acidsand Glycerol

Triglyceride

Adipose Cells

Insulin Deficiency

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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

• 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 and terbutaline)

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 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 DKAINSULIN 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 DKAPOTASSIUM 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 NON-

KETOTIC 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, 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 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

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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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