+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.