1. Diabetic Ketoacidosis
DKA
Diabetic Ketoacidosis

2. Definition
Diabetic ketoacidosis (DKA) is a potentially life-threatening complication in patients with diabetes mellitus. It happens predominantly in those with type 1 diabetes. It occurs when the body cannot use sugar (glucose) as a fuel source because there is no insulin or not enough insulin. The body then breaks down fat to use for fuel. When fat breaks down, waste products called ketones build up in the body.

3. causes Undiagnosed diabetes Poor compliance with Insulin therapy
Omission of Insulin
Infection
Illness
Pregnancy MI
Stroke
Alcohol/drug use
Fever
Surgery
Trauma or overwhelming stress
Mismanagement of sick days
DKA most frequently occurs in those who already have diabetes. It may also be the first presentation in someone who had not previously been known to be diabetic. There is often a particular underlying problem that has led to the DKA episode. This may be intercurrent illness (pneumonia, influenza, gastroenteritis, a UTI), pregnancy, inadequate insulin administration (e.g. defective insulin pen device), heart attack, stroke or the use of cocaine. Many diabetics stop insulin altogether when they are not eating when they actually need more insulin.

4. complications Heart Attack Bowel ischemia/death Renal Failure Death
Heart attack from hypovolemia, potassium abnormalities
Bowel ischemia/death, renal failure from hypovolemia and hypotension
Death ranges from 1%-10%. Shock or coma on admission indicates a worse prognosis
Main cause of death are circulatory collapse, hypokalemia, and infection.

5. Mechanism
Diabetic ketoacidosis arises because of absolute lack of insulin in the body.
The lack of insulin and corresponding excess of glucagon leads to increased release of glucose by the liver (a process that is normally suppressed by insulin) from glycogen and through gluconeogenesis
Although serum glucose levels remain high, glucose is unable to enter the cell; the body cells continue to send signals to stimulate glucose production.
Fat is broken down as a source of glucose and partially oxidized fatty acids build up in the serum.
High glucose levels spill over into the urine, taking water and solutes (such as sodium and potassium) along with it in a process known as osmotic diuresis.
Diabetic ketoacidosis arises because of absolute lack of insulin in the body.
The lack of insulin and corresponding excess of glucagon leads to increased release of glucose by the liver (a process that is normally suppressed by insulin) from glycogen and through gluconeogenesis. (is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates such as lactate, glycerol, and glucogenic amino acids.)
Although serum glucose levels remain high, glucose is unable to enter the cell; the body cells continue to send signals to stimulate glucose production.
Fat is broken down as a source of glucose and partially oxidized fatty acids build up in the serum.
High glucose levels spill over into the urine, taking water and solutes (such as sodium and potassium) along with it in a process known as osmotic diuresis.
The absence of insulin also leads to the release of free fatty acids from adipose tissue; these are converted, again in the liver, into ketone bodies. Ketone bodies, however, have a low pH and therefore turn the blood acidic. (metabolic Acidosis).
The body initially buffers this with the bicarbonate buffering system, but this is quickly overwhelmed and other mechanisms to compensate for the acidosis, such as hyperventilation to lower the blood carbon dioxide levels.
This hyperventilation, in its extreme form, may be observed as Kussmaul respiration. Ketones, too, participate in osmotic diuresis and lead to further electrolyte losses.
The average adult DKA patient has a total body water shortage of about 6 liters (or 100 ml/kg), in addition to substantial shortages in sodium, chloride, phosphate, magnesium and calcium. Glucose levels usually exceed 13.8 mmol/l or 250 mg/dl.

6. Mechanism (cont.)
The absence of insulin also leads to the release of free fatty acids from adipose tissue; these are converted, again in the liver, into ketone bodies. Ketone bodies, however, have a low pH and therefore turn the blood acidic. (metabolic Acidosis).
The body initially buffers this with the bicarbonate buffering system, but this is quickly overwhelmed and other mechanisms to compensate for the acidosis, such as hyperventilation to lower the blood carbon dioxide levels.
This hyperventilation, in its extreme form, may be observed as Kussmaul respiration. Ketones also participate in osmotic diuresis and lead to further electrolyte losses.
The average adult DKA patient has a total body water shortage of about 6 liters (or 100 ml/kg), in addition to substantial shortages in sodium, chloride, phosphate, magnesium and calcium. Glucose levels usually exceed 13.8 mmol/l or 250 mg/dl.
Diabetic ketoacidosis arises because of absolute lack of insulin in the body.
The lack of insulin and corresponding excess of glucagon leads to increased release of glucose by the liver (a process that is normally suppressed by insulin) from glycogen and through gluconeogenesis. (is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates such as lactate, glycerol, and glucogenic amino acids.)
Although serum glucose levels remain high, glucose is unable to enter the cell; the body cells continue to send signals to stimulate glucose production.
Fat is broken down as a source of glucose and partially oxidized fatty acids build up in the serum.
High glucose levels spill over into the urine, taking water and solutes (such as sodium and potassium) along with it in a process known as osmotic diuresis.
The absence of insulin also leads to the release of free fatty acids from adipose tissue; these are converted, again in the liver, into ketone bodies. Ketone bodies, however, have a low pH and therefore turn the blood acidic. (metabolic Acidosis).
The body initially buffers this with the bicarbonate buffering system, but this is quickly overwhelmed and other mechanisms to compensate for the acidosis, such as hyperventilation to lower the blood carbon dioxide levels.
This hyperventilation, in its extreme form, may be observed as Kussmaul respiration. Ketones, too, participate in osmotic diuresis and lead to further electrolyte losses.
The average adult DKA patient has a total body water shortage of about 6 liters (or 100 ml/kg), in addition to substantial shortages in sodium, chloride, phosphate, magnesium and calcium. Glucose levels usually exceed 13.8 mmol/l or 250 mg/dl.

7. symptoms Usually evolve over 24 hour period Nausea & vomiting
Pronounced thirst
Excessive urine production
Abdominal pain
Fruit-scented breath
Weakness/fatigue
Tachycardia
Hypotension
Kussmal Respirations (deep, gasping breaths)
Lethargy, confusion, parasthesia, visual changes
Coma
The symptoms of an episode of diabetic ketoacidosis usually evolve over the period of about 24 hours. Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe
Cardiovascular: Hypotension (osmotic diuresis leads to profound hypovolemia)and tachycardia
EKG: initially potassium is elevated so look for tall, peaked T waves and widening QRS complex.

8. Lab values
Potassium: Initially elevated, then values drop very rapidly with treatment. An ECG may be used to assess the cardiac effects of extremes in potassium levels.
BUN and Creatinine: Levels are elevated.
Anion gap: Elevated >14
Hematocrit elevated due to dehydration
Urine and serum ketone levels elevated
HbA1C (if not done in the last 90 days)
Urinalysis
Beta-Hydroxybutyrate (BHB) >0.27 mmol/L
Serial measurements of Beta-Hydroxybutyrate can be valuable in monitoring the effectiveness of treatment.  Expected normal values for Beta-Hydroxybutyrate are:  0 – 0.27 mmol/L.  Values > 0.27 mmol/L indicate ketosis.
(used instead of serum acetone)
Quantitative Beta-Hydroxybutyrate (BHB) can be used to clinically diagnose and monitor the disease status or severity of diabetes mellitus, alcoholism, glycogen storage disease, high fat/low carbohydrate diets, pregnancy, alkalosis, ingestion of isopropyl alcohol and salicylate poisoning.
When the body begins to break down its stored fats in response to a low supply of energy (glucose) it produces the ketone Beta-Hydroxybutyrate, which is further catabolized into aceoacetate and then into acetone.
Beta-Hydroxybutyrate (BHB) is the most abundant of the physiological ketone bodies (the others being acetone and acetaoacetate).  Lake Health’s previous nitroprusside method (Acetest) only detected 22% of blood ketones present during ketosis.  During ketosis, Beta-Hydroxybutyrate increases more than the levels of acetone and acetaoacetate.

9. Lab values (con’t) Repeat laboratory tests are critical.
Potassium level needs to be checked by drawing a BMP every 2 hours during initial treatment until the potassium is normal. Once the potassium is normal you will draw a BMP every 4 hours x 2 AND anion gap is <14 x 2
Blood Glucose Monitoring will be performed every hour

10. diagnosis Mild DKA: pH <7.30, bicarb level <15 mEq/L
Urine and or serum test for ketones
Blood glucose >250mg/dL
Anion gap >14
Anion gap is the method used to evaluate a patient’s acid-base status; based on the observation that the sum of blood cations (sodium, potassium, chloride, and bicarbonate ions) usually exceeds the sum of the anions (sulfates, phosphates, proteinates, organic acid ions); the difference between the two is the anion gap. Significant departure from the normal level of difference indicates acid-base disturbances. Normal anion gap is 0-16 MMOL/L
Arterial PH < 7.3
Serum Bicarbonate <15
Mild DKA: pH <7.30, bicarb level <15 mEq/L
Moderate DKA: pH <7.2, bicarb <10 mEq/L
Severe DKA: pH <7.1, bicarb <5 mEq/L
Anion gap is the method used to evaluate a patient’s acid-base status; based on the observation that the sum of blood cations (sodium, potassium, chloride, and bicarbonate ions) usually exceeds the sum of the anions (sulfates, phosphates, proteinates, organic acid ions); the difference between the two is the anion gap. Significant departure from the normal level of difference indicates acid-base disturbances. Normal anion gap is 0-16 MMOL/L

11. This is where the ED routinely fails
This is where the ED routinely fails. It is the truest indicator of whether the patient is getting better

12. An 80 kg patient would receive insulin at 11.2 ml/hr
Very Important!
Insulin is a high risk medication and always needs to be checked by 2 RN’s
An 80 kg patient would receive insulin at 11.2 ml/hr

14. education Knowledge deficit related to diabetes management
Review disease process for DKA with patient and family including signs and symptoms
Review insulin administration, glucose monitoring, and “sick day” protocols
Review long term effects of uncontrolled diabetes mellitus
Teach DKA prevention to avoid hospitalization, DKA is preventable!