+ this lecture was conducted during the nephrology unit grand ground by nephrology registrar under...
TRANSCRIPT
+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.
+
Hanan MalSub-intern
Diabetic Ketoacidosis
Overview & Management Protocol
+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
+What is it?
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
Hyperglycemia
>250 mg/dl
Ketonemia
>54 mg/dl
AcidemiapH<7.35
+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
+Pathophysiology
+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
+Presentation
S&S
Urinary systemPolyuria
Ketonuriaglycosuria Gastric
N&VAbdominal Pain
Anorexia
CentralReduced
consciousness
RespiratoryTachypnea
CardiacTachycardia
OtherDehydration
Ketotic Breath
+Investigations
Cardiac monitor
Vital signs q 2hr for 24 hrs
Glucose levels q 1hr
VBG & U&E q 2hr (if K+ >6 or <3 q 1hr)
Calculate anion gap (Na+-(Cl-+HCO3
-)) (8-14)
Urinalysis and Ketones
Input/output chart
CBC w/ differentials
Renal function
CxR (r/o pneumonia)
ECG & cardiac enzymes (ACS?)
+Management
Remember this is an EMERGENCY ABC Insert 2 IV cannula & give NS bolus
We focus on 3 areas of management Fluid Insulin Electrolyte
+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
+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
+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)
+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 10-15 mmol/L in the first 24hrs
Glucose level
<5mmol/L
Infusion rate
by 2U/Hr
Give D50
DO NOT STOP INSULI
N (Keton
es must be
cleared first)
>15mmol/L
Adjust insulin infusion15-18 (1U)18-20 (2U)
>20 (0.1U/Kg bolus + 2U)
+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
+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 replaceme
nt
+BICARBONATE & PHOSPHATE
Bicarbonate 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
+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
+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
+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.
+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.