1. This lecture was conducted during the Nephrology Unit Grand Ground by Nephrology Registrar under Nephrology Division, Department of Medicine in King Saud University. Nephrology Division is not responsible for the content of the presentation for it is intended for learning and /or education purpose only.

2. Diabetic Ketoacidosis
Overview & Management Protocol
Hanan Mal Sub-intern

3. Objectives Understand the action of insulin on the body
Understand the mechanism of DKA and why it happens
Understand the management protocol for DKA
Understand the complications of DKA management

4. What is it? Ketonemia Acidemia An acute complication of Diabetes
Hyperglycemia
>250 mg/dl
Ketonemia
>54 mg/dl
Acidemia
pH<7.35
An acute complication of Diabetes
A state of absolute or relative insulin deficiency
Diagnostic Criteria:
Glucose >14mmol/L
Ketonuria(2+) & Ketonemia (>3mmol/L)
pH <7.35 and HCO-3 <15mEqu/L

5. Pathophysiology Insulin is anabolic Stores glucose (as glycogen)
Protein formation
Stores fats (as TG)
Lack of insulin leads to increased counter-regulatory hormones (catabolic)
Increased insulin resistance
Glycogenolysis
Proteolysis and gluconeogenesis
Lipolysis into FFA and Ketone bodies

6. Pathophysiology

7. Precipitating Factors
STRESS
Non-Compliance
Infections (pneumonia & UTI)
New Onset DM
Co-morbidities
Drug abuse
Emotional/psych stress
Recent Surgeries/ Trauma
Drugs that affect carb metabolism

8. Reduced consciousness
Presentation
S&S
Urinary system
Polyuria
Ketonuria
glycosuria
Gastric
N&V
Abdominal Pain
Anorexia
Central
Reduced consciousness
Respiratory
Tachypnea
Cardiac
Tachycardia
Other
Dehydration
Ketotic Breath

9. Investigations Cardiac monitor Input/output chart
Vital signs q 2hr for 24 hrs
CBC w/ differentials
Glucose levels q 1hr
Renal function
VBG & U&E q 2hr (if K+ >6 or <3 q 1hr)
CxR (r/o pneumonia)
ECG & cardiac enzymes (ACS?)
Calculate anion gap (Na+-(Cl- +HCO3-)) (8-14)
Urinalysis and Ketones

10. Management Remember this is an EMERGENCY
ABC
Insert 2 IV cannula & give NS bolus
We focus on 3 areas of management
Fluid
Insulin
Electrolyte

11. FLUID Adults may lose up to 6L
Aim to replace fluid over 48hrs and replace any urine output
The main aims for the first few liters of fluid replacement
correct hypotension by restoration of circulatory volume
clear ketones
correct electrolyte imbalance

12. FLUID 1L of NS as a bolus over the first 30min
1L over 1hr > 1L over 2hr > 1L over 4hr …
If glucose is <14mmol/L we give D5 NS
EXCEPT:
Signs of heart failure or renal failure we give small boluses of IV fluids or a slower infusion rate
Hyernatremia (Na+>150mmol/L) we give ½ NS instead
If patient is <60Kg we consider less fluid

13. INSULIN Only start insulin once…
the first bolus of fluid is given to avoid vascular collapse secondary to sudden fluid shift into ICS
K+ levels are greater than 3.3mEq/L, otherwise insulin will mediate the movement of K+ intracellularly and worsen hypokalemia
Insulin therapy improves hyperglycemia (inhibits gluconeogenesis) & ketosis & acidosis (inhibits ketone production and lipolysis)

14. INSULIN The standard regimen is 0.1 U/Kg/Hr Our goal is:
Achieving a rate of decline of 3-4 mmol/hr
Maintain glucose between mmol/L in the first 24hrs
Glucose level
<5mmol/L
 Infusion rate by 2U/Hr
Give D50
DO NOT STOP INSULIN (Ketones must be cleared first)
>15mmol/L
Adjust insulin infusion
15-18 (1U)
18-20 (2U)
>20 (0.1U/Kg bolus + 2U)

15. INSULIN
Discontinue IV insulin only when the patient meets the following criteria:
Anion gap is <12mEq/L
HCO3- >19mEq/L
Patient is tolerating oral feed
Subcutaneous insulin has been initiated for 2hrs or more

16. POTASSIUM Potassium levels should be monitored Q 2hrs
<3mEq/L add 60mEq KCl/h
3-4mEq/L add 40mEq KCl/h
4-5.9mEq/L add 20mEq KCl/h
K+ Level
> 5.9 or Renal Failure
DO NOT START K+ REPLACEMENT
<3
Hold insulin replacement

17. BICARBONATE & PHOSPHATE
No evidence to support
If pH <6.9 & patient is shocked give 1mEq/Kg IV over 2hr
HCO3- can precipitate hypokalemia thus we add 20mEq KCl to infusion
Phosphate
No evidence shows clinical benefit
May lead to hypocalemia
Indicated to avoid cardiac dysfunction, skeletal muscle weakness & respiratory depression

18. Complications of Management
Treatment for DKA has to be done by a trained specialist
Constant monitoring of the patient is required to avoid development of complications
Transfer patients to resuscitation if,
Patient develops coma or impaired consciousness
Hemodynamic instability
pH <7.1 and HCO3- <5
K+ >6.5 or <3

19. Complication Cause Hypoglycemia
Over administration of insulin (High dose regimen 1U/Kg)
Hypokalemia
Secondary to high dose regimen insulin (1U/Kg) and HCO3-
Hyperglycemia
Discontinuation/ interruption to insulin treatment
Hyperchloremia
Excessive saline administration
Cerebral Edema
Most fatal
Possible contributors:
hypoxia
movement of water into the CNS with rapid fall in plasma osmolality
effect of insulin on the plasma membrane of brain cells, which may promote cellular edema
Fluid Overload
Patients with cardiac failure or renal insufficiency may develop CHF
ARDS
Due to Pulmonary edema
Thromboembolism
Enhancement of the hypercoagulable state of a DM patient

20. Summery DKA is a common complication that will be met in any ER
DKA can be easily diagnosed by asking the right questions and catching the right signs
DKA can be easily managed if the protocol for management is followed correctly
Complications can be avoided by making sure a trained specialist is present and monitoring is done correctly.

21. References
Michelle A. Charfen, MD, Madonna Fernandez-Frackelton, MD, FACEP. Diabetic Ketoacidosis. Emerg Med Clin N Am 23 (2005) 609–628
Faiza A. Qari, FRCP, ABIM. Precipitating Factors for Diabetic Ketoacidosis. Saudi Med J 2002; Vol. 23 (2).
M. W. Savage, et al. Diabetes UK Position Statements and Care Recommendations, Joint British Diabetes Societies guideline for the Management of Diabetic Ketoacidosis. Diabetic Medicine, 2011.
Dr, Hani Ibrahim, Dr. Anwar Jammah. DKA Protocol. KKUH department of Emergency Medicine.