DIABETIC KETOACIDOSISIN ICU

PRESENTED BY:

DR. ZEENAT YASMEEN ICU RESIDENT

Diabetic Ketoacidosis (DKA)A state of absolute or relative insulin deficiency aggravated and followed byhyperglycemia, dehydration, and acidosis-producing derangements in metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II DiabetesIn type II diabetics with insulin deficiency/dependenceIt is the presenting symptom for ~ 25% of Type I Diabetics.

Definition of Diabetic Ketoacidosis**

Pathogenesis of DKAInsulinDeficiencyBeta-cellfailureD/CInsulin Glucotoxicity

Insulindeficiency

IncreasedglucagonGHcortisolcatecholaminesPathogenesis of DKA

Carbohydrate Metabolism in DKA Relative or absolute insulin deficiencyglucose output

glycogenolysisliverglucose uptakemuscle

Increased Glucose Production in DKA

Increased Production of Ketones in DKALipolysisFFAGlycerolKetogenesisB-OH-BAcetoacetate

TG

Diagnostic Criteria for DKA DKA Mild Moderate SeverePlasma 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>2507.0-1210- 25012

Clinical Presentation of DKASignHypothermiaTachycardiaTachypneaKussmaul breathingIleusAcetone breathAltered sensoriumSymptomsPolydipsiaPolyuriaWeaknessWeight lossNausea Vomiting Abdominal painThe 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)AlcoholStrokeMyocardial InfarctionPancreatitisTraumaMedications (steroids)Non-compliance with insulin

Initial Clinical EvaluationHistory and physical examinationSecure patients ABCMental statusCardiovascular-renal statusSource of infection

Evaluation of volume and hydration statusLaboratory studies

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

Laboratory studies:ABGsCBC with differentialCMP (glucose, electrolytes, bicarbonate, BUN, creatinine)Serum ketonesUrinalysis Bacterial cultures*Cardiac enzymes*

Initial Laboratory Studies* If clinically indicated

Serum Sodium

Hyponatremia is common in patients with DKA

H2OH2OH2ONa+H2OCorrection 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+K+Insulinregulates Activity ofNa+/K+ pumpNa+K-

K+K+K+

Anion Gap FormulaAnion gap can be measured as

AG=[(Na)-(Hco3+CL)]

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 in DKA

Caution during fluid managementFluid 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 DKACheck initial blood glucose q1h.Goal decrease in blood glucose is 50-75mg/dl/hrOnce 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

Intravenous Insulin Therapy in DKA

CHANGING THE INSULIN INFUSION RATEDecrease IV insulin by 50%if blood glucose decrease by >100mg/dl/hr in any 1hr periodIncrease insulin drip by 50%/hr if change in blood glucose is

Transition to Subcutaneous InsulinPatients with DKA should be treated with IV insulin until ketoacidosis is resolved.

Criteria for resolution of DKA:BG 200 mg/dLSerum bicarbonate level 18 mEq/LVenous pH 7.3 and anion gap closed

WHEN TO STOP IV INSULINGive 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

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 ketoacidosisSummary

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