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Diabetic Ketoacidosis Written Report

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DIABETIC KETOACIDOSIS (a.k.a. DKA)

I. Introduction

Diabetic Ketoacidosis (DKA) is an acute complication of Type I DM that is characterized by uncontrolled lypolysis, ketogenesis, hyperkalemia and other electrolyte imbalances and metabolic acidosis.

DKA is more common in young ( 300 mEq/24 hours. Despite a significant total body deficit of Potassium, initial serum Potassium is typically normal or elevated because of the extracellular migration of Potassium in response to acidosis. Potassium levels generally fall further during treatment as insulin therapy drives potassium into cells. If serum potassium is not monitored and replaced as needed, lifethreatening hypokalemia may develop.

Compensatory Attempts Excessive ketone production causes metabolic acidosis. DKA occurs when the increased production of ketoacids overwhelms attempts at compensation. The rapid overproduction of ketoacids depletes the buffering effect bicarbonate and results in acidosis. The body uses three defense mechanisms in an attempt to

counter impending acidosis: (1) respiratory compensation, (2) intracellular buffering, and (3) renal correction.19,32 Excess carbon dioxide is exhaled to correct the metabolic acidosis. This results in tachypnea or Kussmauls respiration. In addition, buffering occurs when excess hydrogen ions move intracellularly in exchange for potassium ions to maintain a neutral intracellular charge. The kidneys attempt to correct ketoacidosis by increasing the excretion of ketoacids. Acidosis will continue to worsen if not corrected by the administration of insulin.

Insufficient/Absence of Insulin Infection Undiagnosed/Untreated type 1 DMCellular Cellular Starvation Starvation Secretion of counterregulatory hormones such as: catecholamines, glucagon, cortisol and growth hormone Stimulation of hunger mechanism via hypothalamus Hung er Polyphagi Polyphagi a a Glucogenolysi s Glucose

Lypolysis Release of Fatty Acids to liver Ketogenes is Ketones Ketones formation formation Accumulation of Hydroxybuterate and Acetone Acetic acid in the blood Metabolic Metabolic Acidosis Acidosis Abdominal Abdominal Pain Pain

Fat content in the blood Hyperlipide mia Formation of fats on the walls of BV Atherosclero Atherosclero sis sis

Proteolysis Amino acid production Gluconeogen esis Hyperglyce Hyperglyce mia mia Osmotic Diuresis Polyuri Polyuri a a Glycosuri Glycosuri a a Dehydratio Dehydratio n n Hypovolem ia Thirst

Hyperosmolal ity Polydyps Polydyps ia ia

Ketonuria Ketonuria

N/V Poor Poor appetite appetite Weight Weight loss loss Weaknes Weaknes s s

Cellular K+ Arrhythmi Arrhythmi as as

Body attempts to prevent further in pH Kussmaul Kussmaul s s respiration respiration Acetone Acetone breath breath

Depressed Depressed CNS CNS Headac Headac he he Com Com a a

BP Shoc k

III. Diagnostic Procedures

Initial diagnosis of DKA: serum glucose level >11mmol/L, acidaemia, and presence of ketones in urine6 Blood sugar level (BSL) hourly measures. Initial blood glucose

levels can be as high as 30-45mmol/L. Arterial blood gas (ABG) to measure degree of acidosis and

degree of compensatory hypocarbia (PaCo2). Initially arterial pH, but following pH can be venous as venous pH correlates well with arterial pH3 (venous pH is usually 0.03 units lower than arterial pH). When pH drops below 7.2 hyperventilation and hypocarbia are more pronounced. Serum bicarbonate