Dka pathphysiologymanagement2014-copy-140202235658-phpapp02

DIABETIC KETOACIDOSISIN ICU

PRESENTED BY:

DR. ZEENAT YASMEEN ICU RESIDENT

Diabetic Ketoacidosis (DKA)

• A state of absolute or relative insulin deficiency aggravated and followed by

• hyperglycemia, dehydration, and acidosis-producing derangements in metabolism, including production of serum acetone.

• Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence

• It is the presenting symptom for ~ 25% of Type I Diabetics.

Hyperglycemia

Ketosis

Acidosis

*

Definition of Diabetic Ketoacidosis*

3

Pathogenesis of DKA

InsulinDeficiency

Beta-cellfailure

D/CInsulin

Glucotoxicity

Insulindeficiency

IncreasedglucagonGHcortisolcatecholamines

Pathogenesis of DKA

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

Adiposetissue

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

Initial Clinical Evaluation

• History and physical examination Secure patient’s ABC Mental status Cardiovascular-renal status Source of infection

• Evaluation of volume and hydration status

• Laboratory studies

• 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

Serum Sodium

Hyponatremia is common in patients with DKA

H2O

H2OH2O

Serum glucose

Na+

H2O

Correction of Serum sodium:

Corrected Na+ = [Na+] 1.6 x glucose (mg/dl) – 100

100

Serum Potassium

Admission serum potassium is frequently elevated (due to a shift of K- from the intracellular to the extracellular space)

K+

OsmolalityAcidosis

K+

Insulinregulates Activity

ofNa+/K+ pump

Na+

K-

K+

K+K+

Anion Gap Formula

• Anion gap can be measured as

• AG=[(Na)-(Hco3+CL)]

Fluid Therapy in DKA

Normal saline, 1-2 L over 1-2 h

NS or ½ NS at 250-500 mL/h

Glucose < 250 mg/dl

D5%1/2NS saline

Caution during fluid management

• Fluid should be replace over 12-24hr • patients are generally depleted 3-6lit in

DKA.• Monitor urine output,heart rate,blood

pressure and respiratory status.• CARE must b taken in patient with CCF

and kidney disease.

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.

Intravenous Insulin Therapy in DKA

I.V. Bolus: 0.1 U/kg

I.V. drip: 0.1 U/kg/h

Glucose < 250 mg/dl and HCO3 > 15 mmol/l, then,

I.V. drip: 0.05 – 0.1 U/kg/h Until c0rrection of anion gap

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

• Give short acting insulin SC at twice the hourly IV rate(if iv rate 5u/hr give 10u)

• Failure to give SC insulin may result in rebound hyperglycemia and ketosis due to its short acting effect.

• ENSURE pt has a meal and is eating and awake.

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

pH > 7.0 no bicarbonate

pH < 7.0 and bicarbonate < 5 mEq/l 44.6 mEq in 500 ml 0.45% saline over 1 h until pH > 7.0

Bicarbonate administration

Complications of DKA 1-Complications of associated illnesses e.g.

sepsis or MI.2-Adult respiratory distress syndrome. 3-Thromboembolism (elderly). 4-Complications of treatment:

a-Hypokalemia: Which may lead to:

-Cardiac arrhythmias.

-Cardiac arrest.

-Respiratory muscle weakness.

b-Hypoglycemia.

c-Overhydration and acute pulmonary edema: particularly in:

-Treating children with DKA.

-Adults with compromised renal or cardiac function.

-Elderly with incipient CHF.

d-Neurological complications: Cerebral Edema.

-It occurs mostly in children with DKA.

-Very dangerous and increases mortality.

-The risk is related to the severity, duration and rapid correction of DKA.

 Mechanism: The brain adapts by producing

intracellular osmoles (idiogenic osmoles) which stabilize the brain cells from shrinking while the DKA was developing. When the hyperosmolarity is rapidly corrected, the brain becomes hypertonic towards the extracellular fluids water flows into the cells cerebral edema

Diabetic Ketoacidosis is a common, serious and expensive complication in patients with type 1 and type 2 diabetes

Prevention of metabolic decompensation through patient education, strict surveillance of glucose homeostasis and aggressive diabetes management might reduce the high morbidity and mortality associated with diabetic ketoacidosis

Summary

THANK YOU