Presentation is loading. Please wait.

Presentation is loading. Please wait.

Diabetic Ketoacidosis

Similar presentations


Presentation on theme: "Diabetic Ketoacidosis"— Presentation transcript:

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

2 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

3 Diabetic Ketoacidosis
Pathophysiology Diagnosis Treatment Complications of treatment When the acidosis is resolved

4 Diabetic Ketoacidosis
Abnormal metabolic state Due to insulin deficiency In patient with type 1 diabetes Characterized by hyperglycemia and acidosis

5 Hyperglycemia Ketone production
Ketone utilization Osmotic diuresis HYPERKETONEMIA DEHYDRATION vomiting Decreased GFR Hydrogen ion production exceeds utilization ACIDOSIS

6 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

7 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

8 Physical Exam Signs of dehydration Kussmaul type breathing
Acetone odor Blood pressure and pulse Temperature Ileus and gastric atony State of consciousness

9 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

10 Laboratory 2 Anion gap elevated: Na- (Cl + HCO3)
Creatinine spuriously elevated Hemoglobin and hematocrit elevated WBC may be elevated

11 Therapy 1. Correction of the dehydration (PRIORITY)
2. Correction of the hyperglycemia

12 Dehydration Immediately decreases levels of “anti-insulin” hormones
Insulin resistance exacerbates the insulin deficiency Rehydration will decrease stress hormones Rehydration will improve kidney perfusion

13 Dehydration DKA is a hypertonic state and should be corrected over hours If clinically in shock, cc/kg .9NS or plasma expander over 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

14 Dehydration Deficit replacement should be given EVENLY over 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

15 Insulin Regular (novolog) insulin U100 0.05 - .1U/kg/hr
If glucose is < mg/dl and acidosis is persisting, it is better to increase the glucose in the infusion rather than decrease the insulin

16 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

17 Complications of therapy
Hypokalemia Inadequate rehydration Hypoglycemia Cerebral edema and other CNS catastrophes

18 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

19 Inadequate Rehydration

20 Hypoglycemia

21 Cerebral edema Paradoxical development of CSF and CNS acidosis
Altered CNS oxygenation Unfavorable osmotic gradients A decline in the true sodium

22 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

23 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

24 Cerebral Edema Prevention
Slow rehydration with slow changes in osmolality Serum sodium should rise as serum glucose falls Hourly mental status checks

25 After Resolution IV insulin until it is time for meal
Twice daily short acting/intermediate acting insulin (or usual insulin dose) Approximately .75 units/kg 2/3’s in am; 1/3 in pm 2/3’s intermediate acting; 1/3 short acting Lunch: .2 units/kg short acting

26 Team Management Physician Certified diabetes educator Dietician
Psychologist or social worker

27 Insulin Rapid acting - Humalog or Novolog Short acting - Regular
Intermediate acting - NPH, Lente Long acting - Ultralente New, peakless - Glargine (Lantus)

28 Target Blood Glucose Levels
Prebreakfast Prelunch and dinner Prebedtime snack Younger child mg/dl mg/dl mg/dl mg/dl

29 Principles of Meal Planning
Meet nutritional requirements Well balanced meals and snacks Healthful fat consumption Avoid obesity Incorporate social and cultural factors Artificial sweeteners

30 Constituents of Meal Plan
Carbohydrate Protein Fat 50-60% calories 15-20% calories 25-35% calories

31 Monitoring Hemoglobin A1c Home glucose monitoring Glucowatch
Subcutaneous sensor

32 Have a good day! good day Have


Download ppt "Diabetic Ketoacidosis"

Similar presentations


Ads by Google