DIABETIC KETOACIDOSIS

PRESENTED BY:

DR. Eyad Hamad Miskawisupervised by : Dr. Eyas Saleh

Hyperglycemia

Ketosis

Acidosis

*

Definition of Diabetic Ketoacidosis*

2

Pathogenesis of DKA

InsulinDeficiency

Beta-cellfailure

D/CInsulin

Glucotoxicity

Carbohydrate Metabolism in DKA

Relative or absolute insulin deficiency

glucose output

glycogenolysis

liver

glucose uptake

muscle

Increased Glucose Production in DKA

Gluconeogenesis Glucose

Protein breakdownLipolysis

Glycerol Amino acids Lactate

TG

Activity of gluconeogenicenzymes (PEPCK, PC, PFK)

Increased Production of Ketones in DKA

Lipolysis

FFA Glycerol

Ketogenesis

B-OH-BAcetoacetate

TG

Pathogenesis of DKA

Liver

Increasedglucose

production

Decreasedglucoseuptake

Peripheraltissue

HYPERGLYCEMIA

Increasedrelease

FFA

Increasedketogenesis

Adipose

tissue

Liver

KETOACIDOSIS

Osmotic diuresis

Volume depletion Metabolic acidosis

Decreased alkali reserve

Diagnostic Criteria for DKA DKA

Mild Moderate Severe

Plasma glucose (mg/dl)pHAnion gap Bicarbonate (mEq/l)Urine ketones*Serum ketones*Effective serum Osmol (mOsm/kg)†Alteration in sensoriaor mental obtundation

>2507.25-7.3 >10 15-18positivepositivevariable

alert

>2507.0-<7.24 >1210- <15positivepositivevariable

alert/drowsy

>250<7.0 >12<10positivepositivevariable

stupor/coma

Clinical Presentation of DKA

SignHypothermiaTachycardiaTachypneaKussmaul breathingIleusAcetone breathAltered sensorium

SymptomsPolydipsiaPolyuriaWeaknessWeight lossNausea Vomiting Abdominal pain

The onset of DKA is usually relative short, ranging from hours to a day or two.

Causes of DKA

• Stressful precipitating event that results in increased catecholamines, cortisol, glucagon. Infection (pneumonia, UTI) Alcohol Stroke Myocardial Infarction Pancreatitis Trauma Medications (steroids) Non-compliance with insulin

• Immediate determination of blood glucose by finger stick, and serum ketones (3-BH) by finger stick or urinary ketones.

• Laboratory studies: ABG’s CBC with differential CMP (glucose, electrolytes, bicarbonate, BUN, creatinine) Serum ketones Urinalysis Bacterial cultures* Cardiac enzymes*

Initial Laboratory Studies

* If clinically indicated

Replacement of fluids lossesCorrection of hyperglycemia/metabolic

acidosisReplacement of electrolytes lossesDetection and treatment of precipitating

causesConversion to a maintenance diabetes

regimen (prevention of recurrence)

Management of DKA

Fluid Therapy

• Assume 10-15% dehydration• Begin with a 10-20 ml/kg bolus of NS• Replace calculated deficit evenly over 36 hours -

generally 1.5 x maintenance for the next several hours is appropriate

• Do not exceed 40ml /kg in the initial 4 hours• Double bag system

NS at 1.5 x M until glucose below 300 mg/dl D10 NS to be mixed with NS to achieve desired

glucose concentration

Insulin bolus ??

•Insulin bolus or not ?• Insulin should be started about an hour after IV fluid

replacement is started to allow for checking potassium levels and because insulin may be more dangerous and less effective before some fluid replacement has been obtained.

• Although the incidence of life-threatening hypokalemia due to aggressive insulin administration is very low, there is little to no advantage in starting insulin prior to rehydration and evaluation of serum potassium levels. Initial bolus of insulin does not change overall management of DKA

Insulin Therapy

• IV infusion with basal rate 0.1 U/kg/hr

• Ideal glucose decline is about 50-100 mg/hr

• Continue insulin until urinary (blood) ketones are cleared and anion gap is closed

Blood Glucose monitoring in DKA

• Check initial blood glucose q1h.Goal decrease in blood glucose is 50-75mg/dl/hr

• Once stable(3consecutie values decrease in target range)change blood glucose monitoringq2h.Resume q1h blood glucose monitoring for each change in the insulin infusion rate.

• Add dextrose5% to IV fluid when blood glucose <250mg/dl.

• For DKA goal blood glucose 150-200mg/dl until anion gap close.

CHANGING THE INSULIN INFUSION RATE

• Decrease IV insulin by 50%if blood glucose decrease by >100mg/dl/hr in any 1hr period

• Increase insulin drip by 50%/hr if change in blood glucose is <50mg/dl/hr

• When blood glucose decrease to 250mg/dl insulin infusion may need to be decrease 50% to maintain glucose at target levels(150-200mg/dl).

Transition to Subcutaneous Insulin

Patients with DKA should be treated with IV insulin until ketoacidosis is resolved.

Criteria for resolution of DKACriteria for resolution of DKA:: BG BG ≤≤ 200 mg/dL 200 mg/dL Serum bicarbonate level ≥ 18 mEq/LSerum bicarbonate level ≥ 18 mEq/L Venous pH ≥ 7.3 and anion gap closedVenous pH ≥ 7.3 and anion gap closed

WHEN TO STOP IV INSULIN

• When the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by the usual subcutaneous (SC) dose of regular insulin.

Potassium replacement

K+ = > 5.5 mEq/l; no supplemental is required

K+ = 4 - 5 mEq/l; 20 mEq/L of replacement fluid

K+ = 3 - 4 mEq/l; 40 mEq/L of replacement fluid

If admission K+ = <3 mEq/l give 10-20 mEq/h until K+ >3 mEq/l, then add 40 mEq/L to replacement fluid

Sodium

Pseudohyponatremia, add 1.6 mEq of Na to every 100mg/dL of glucose above normal Expect that the Na+ level will rise during treatmentIf Na+ does not rise, true hyponatremia may be present (risk

of cerebral edema) and should be treated

Bicarbonate

• Bicarbonate should be used only when there is severe depression of the circulatory system or cellular metabolism

• Not recommended unless pH <7.0 and bicarbonate < 5 mEq/l, not even then, unless above true

∀ → 44.6 mEq in 500 ml 0.45% saline over 1 h until pH > 7.0

• Bicarbonate administration leads to increased cerebral acidosis

• HCO3- + H+ = CO2 + H2O.

Bicarbonate passes the BBB slowly

CO2 diffuses freely

exacerbating cerebral acidosis and cerebral depression

Bicarbonate

• Bicarbonate should be used only when there is severe depression of the circulatory system or cellular metabolism

• Not recommended unless pH <7.0, not even then, unless above true

• Bicarbonate administration leads to increased cerebral acidosis

• HCO3- + H+ = CO2 + H2O.

Bicarbonate passes the BBB slowly

CO2 diffuses freely

exacerbating cerebral acidosis and cerebral depression

• A 10 y/o male (~30 kg) presents to the ED with a one-day history of emesis and lethargy.

• Vitals show T 37C, HR 110, RR 25, BP 99/65. Patient is lethargic, but oriented. Exam reveals the odor of acetone on the breath, dry lips, but otherwise unremarkable

• Labs: pH 7.05, PaCO2 20, HCO3 9 , PaO2 100, BE -20, Na+ 133, K + 5.2, Cl 96, CO2 8, BS 600. Urine shows 4+ glucose and large ketones

Case Scenario #1

• How much fluid would you administer as a bolus?• What is the value of anion gap ? • Would you administer bicarbonate?• What is the “true” serum sodium?• How much insulin would you administer?• What IVF would you start? At what rate?

Case Scenario #1

Answers

• 600 cc over 20 min• 28 high• No cardiovascular collapse and therefore

there is no justification for the administration of bicarbonate.

• 133 +(600-100)= 142• 0.1*30= 3u/hr• 1.5*(10*100+10*50+10*20)= 2550cc q 24 hrs

Pearls on DKA• Diagnosis : pH < 7.3 , RBS > 300, Hco3 < 15• Correct dehydration over 48 hours • Bolus fluid only with hemodynamic

compromise • Sodium bicarbonate when pH <7.0 and Hco3

< 5 and circulatory compromised .• No rule of insulin bolus .• Monitor K level while you are treating .• Remember to find the cause and treat it.

THANK YOU