Diabetic Ketoacidosis Irene N. Sills, MD Albany Medical Center Albany, NY.

Diabetic Ketoacidosis

Irene N. Sills, MD

Albany Medical Center

Albany, NY

Diabetic Ketoacidosis

Presentation of new onset diabetes about 30% of the time

Is a life-threatening emergency

The metabolic abnormalities must be corrected in a careful, vigilant fashion

Diabetic Ketoacidosis

• Pathophysiology

• Diagnosis

• Treatment

• Complications of treatment

• When the acidosis is resolved

Diabetic Ketoacidosis

• Abnormal metabolic state

• Due to insulin deficiency

• In patient with type 1 diabetes

• Characterized by hyperglycemia and acidosis

Hyperglycemia Ketone production

Ketone utilization

Osmotic diuresis HYPERKETONEMIA

DEHYDRATION vomiting

Decreased GFR

Hydrogen ion production

exceeds utilization

ACIDOSIS

Endogenous Compensation for Acidosis

• Chemical buffering by extracellular (bicarbonate) and intracellular buffers (protein, organic and inorganic phosphates, hemoglobin)

• Control of CO2 levels by alveolar ventilation rate

• Control of blood bicarbonate concentration by changes in H+ excretion (excretion of titrable acidity and ammonium) and reabsorption of bicarbonate

Diabetic Ketoacidosis

• Failure to take insulin (total insulin deficiency)

• Relative insulin deficiency– infection

– trauma

– surgery

– stress

– dehydration **

• Hormones that lower glucose: INSULIN

• Hormones that raise glucose: catecholamines, cortisol, glucagon, growth hormone

Physical Exam

• Signs of dehydration

• Kussmaul type breathing

• Acetone odor

• Blood pressure and pulse

• Temperature

• Ileus and gastric atony

• State of consciousness

Laboratory 1

• Glucose 400-500 mg/dl, but may vary

• Arterial pH less than 7.3; bicarbonate less than 15mM/L

• Sodium usually normal, but may be low

• Potassium initially elevated

• Serum ketones positive

• Serum osmolality elevated

Laboratory 2

• Anion gap elevated: Na- (Cl + HCO3)

• Creatinine spuriously elevated

• Hemoglobin and hematocrit elevated

• WBC may be elevated

Therapy

• 1. Correction of the dehydration (PRIORITY)

• 2. Correction of the hyperglycemia

Dehydration

• Immediately decreases levels of “anti-insulin” hormones

• Insulin resistance exacerbates the insulin deficiency

• Rehydration will decrease stress hormones

• Rehydration will improve kidney perfusion

Dehydration• DKA is a hypertonic state and should be

corrected over 36-48 hours

• If clinically in shock, 10-20 cc/kg .9NS or plasma expander over 30-45 minutes

• Fluids should be no more hypotonic than .45 NS

• Maintenance fluid may be .9NS until serum glucose is less than 300 mg/dl when glucose containing solution is added

Dehydration

• Deficit replacement should be given EVENLY over 36-48 hours

• IV infusion rate usually calculates to one and a-half times maintenance

• On-going losses should be replaced• Potassium should be added when patient

voids• Bicarbonate is usually not needed

Insulin

• Regular (novolog) insulin U100

• 0.05 - .1U/kg/hr

• If glucose is <120-180 mg/dl and acidosis is persisting, it is better to increase the glucose in the infusion rather than decrease the insulin

Monitoring

• Serum glucose hourly

• Electrolytes, calcium, phosphorous every 2-4 hours

• Flowsheet with accurate I’s and O’s, vital signs, insulin doses, mental status checks, and laboratory results

Complications of therapy

• Hypokalemia

• Inadequate rehydration

• Hypoglycemia

• Cerebral edema and other CNS catastrophes

Hypokalemia

• Vomiting

• Renal losses exacerbated by hyperaldosteronism

• Insulin and pH correction moves potassium into the cells

• Danger if the initial potassium is less than 3.6 meq/L

Inadequate Rehydration

Hypoglycemia

Cerebral edema

• Paradoxical development of CSF and CNS acidosis

• Altered CNS oxygenation

• Unfavorable osmotic gradients

• A decline in the true sodium

Cerebral Edema

• Develops 4-12 hours after therapy begun

• Biochemically all is well

• If early mental status changes are not noticed, a child will develop neurologic changes leading to herniation and compromised cardiorespiratory status

Cerebral Edema

• NEJM: Cerebral edema that was not clinically expected developed in a small group of children

• CT scans while in DKA and after resolution

• Ventricular narrowing during therapy

• Perhaps, some degree of swelling in all children

Cerebral EdemaPrevention

• Slow rehydration with slow changes in osmolality

• Serum sodium should rise as serum glucose falls

• Hourly mental status checks

After Resolution

IV insulin until it is time for mealTwice daily short acting/intermediate acting insulin (or usual insulin dose)Approximately .75 units/kg2/3’s in am; 1/3 in pm2/3’s intermediate acting; 1/3 short actingLunch: .2 units/kg short acting

Team Management• Physician

• Certified diabetes educator

• Dietician

• Psychologist or social worker

Insulin• Rapid acting - Humalog or

Novolog

• Short acting - Regular

• Intermediate acting - NPH, Lente

• Long acting - Ultralente

• New, peakless - Glargine (Lantus)

Target Blood Glucose Levels

• Prebreakfast

• Prelunch and dinner

• Prebedtime snack

• Younger child

• 70 - 120 mg/dl

• 70 - 150 mg/dl

• 90 - 180 mg/dl

• 80 - 180 mg/dl

Principles of Meal Planning

• Meet nutritional requirements

• Well balanced meals and

• snacks

• Healthful fat consumption

• Avoid obesity

• Incorporate social and cultural factors

• Artificial sweeteners

Constituents of Meal Plan

• Carbohydrate

• Protein

• Fat

• 50-60% calories

• 15-20% calories

• 25-35% calories

Monitoring• Hemoglobin A1c

• Home glucose monitoring

• Glucowatch

• Subcutaneous sensor

Have Have a good day!

good day