Diabetic Ketoacidosis

DIABETIC KETOACIDOSIS
TABLE OF
CONTENT
• INTRODUCTION
• DEFINITION
• DIAGNOSIS
• EPIDEMIOLOGY
• PATHOPHYSIOLOGY
• ETIOLOGY
• CLINICAL PRESENTATION
• LABORATORY EVALUATION
• MANAGEMENT
• COMPLICATIONS
INTRODUCTIO
N
• Diabetic Ketoacidosis is an acute, major, life-threatening complication

of Diabetes.
• It mainly occurs in patients with Type 1 Diabetes but it is not
uncommon in some patients with Type 2 diabetes.
• Described by Dr. Julius Dreschfeld in 1886.
DEFINITIO
N
• DKA is an extreme metabolic state caused by insulin deficiency. It is

defined as an acute state of severe uncontrolled diabetes associated
with ketoacidosis that requires emergency treatment.
• It is a state of absolute or relative insulin deficiency aggravated by
ensuing hyperglycemia, dehydration and acidosis-producing
derangements in intermediary metabolism.
DIAGNOSI
S
• Triad of hyperglycemia, high anion gap metabolic acidosis and
ketonemia.
ADA (2009)
• Glucose> 13.9 mmol/L (250 mg/dl).
• Bicarbonate< 18mmol/L; pH< 7.3.
• Ketones positive result for urine or serum ketones by nitroprusside
reaction.
JBDS (2013)
• Glucose> 11 mmol/L (200 mg/dl) or known Diabetes.
• Bicarbonate< 15mmol/L or pH< 7.3 or both.
• Ketones> 3mmol/L or (++) in urine dipstick.
EPIDEMIOLO
GY
• DKA accounts for 14% of all hospital admissions of patients with

diabetes and 16% of all diabetes-related fatalities.
• DKA is frequently observed in diagnosis of type 1 diabetes and often
indicates this diagnosis (3%).
• The overall mortality rate for DKA is 0.2-2%, being at the highest in
developing countries.
• The incidence of DKA in developing countries is higher.
• It is far more common in young patients.
ETIOLOGY
• Inadequate insulin treatment or noncompliance.
• New onset diabetes (20-25%)
• Acute illness
• Infection (30 to 40%)
• CVA
• Acute Myocardial Infarction
• Acute Pancreatitis
• Drugs
• Clozapine or olanzapine
• Cocaine
• Lithium
• SGLT2 inhibitors
• Terbutaline
CLINICAL PRESENTATION:
SYMPTOMS
• DKA usually evolves rapidly, over a 24 hour period.

• Earliest symptoms are polyuria, polydipsia and weight loss.
• Nausea, vomiting and abdominal pain are usually present.
• Malaise, generalized weakness and fatigability.
• As the duration of hyperglycemia progresses, neurologic symptoms,
including lethargy, focal signs, and obtundation can develop. Frank
coma is uncommon in DKA.
CLINICAL PRESENTATION:
SIGNS
• Ill appearance.
• Labored respiration (Kussmaul).
• Dry mucous membranes, dry skin and decreased skin turgor.
• Decreased reflexes.
• Characterstic ketotic breath odor.
• Tachycardia
• Hypotension
• Tachypnea
• Hypothermia/ Fever (if infection is present)
• Confusion
• Coma
• Abdominal tenderness.
LABORATORY EVALUATION
• Blood test for glucose every 1-2 hour.
• ABG/ VBG.
• Serum electrolytes (includes phosphate)
• Renal function test.
• Urine dipstick test (acetoacetate).
• Serum ketones (3-hydroxybetabutyrate).
• CBC.
• Anion gap.
• Osmolarity.
• Cultures.
• Amylase.
Repeat lab investigations are key!
MANAGEMEN
T
• Correction of fluid loss with intravenous fluids.

• Correction of hyperglycemia with insulin.
• Correction of electrolyte disturbances, particularly potassium loss.
• Correction of acid-base balance.
• Treatment of concurrent infection, if present.
MANAGEMENT
ALGORITHM
CORRECTION OF FLUID
LOSS
• It is a critical part of treating patients with DKA.
• Use of isotonic saline.
• 15-20mL/kg/hour for the first few hours.
• Recommended schedule:
• Administer 1-3 L during first hour.
• Administer 1 L during second hour.
• Administer 1 L during the following 2 hours.
• Administer 1 L every 4 hours, depending on the degree of dehydration and
CVP.
• When patient becomes euvolemic, switch to 0.45% saline is
recommended, particularly if hypernatremia exists.
INSULIN
THERAPY
• Insulin therapy to be initiated only if potassium levels are above 3.3 mEq/L.
• Intravenous regular insulin preferred.
• Initiated with IV bolus of regular insulin (0.1 units/kg) followed by continuous
infusion of regular insulin of 0.1 units/kg/hour.
• SC route may be taken in uncomplicated DKA (0.3 U/kg then 0.2 U/kg one
hour later).
• When serum glucose reaches 200 mg/dl, reduce insulin infusion to 0.02-
0.03
U/kg/hour and switch the IV saline solution to dextrose in saline.
• Revert to SC insulin, after patient begins to eat (continue IV infusion
simultaneously for 1 to 2 hours).
POTASSIUM
REPLACEMENT
• If the initial serum potassium is below 3.3 mEq/L, IV potassium chloride

is started with saline (20 to 40 mEq/hour).
• If the initial serum potassium is between 3.3 and 5.3 mEq/L, IV KCl (20
to 30 mEq) is added to each liter of IV replacement fluid and continued
until the serum potassium concentration has increased to the 4.0 to 5.0
mEq/L range.
• If the serum potassium is initially greater than 5.3 mEq/L, then
potassium replacement should be delayed.
CORRECTION OF
ACIDOSIS
• Bicarbonate therapy is a bone of contention among physicians and still

remains a controversial subject, as clear evidence of benefit is lacking.
• Bicarbonate therapy is only administered if the arterial pH is less than
6.9.
• 100 mEq of sodium bicarbonate in 400 mL sterile water is administered
over two hours. Repeat doses until pH rises above 7.0.
• Bicarbonate therapy has several potential harmful effects.
COMPLICATIONS
• CVT
• Myocardial Infarction
• DVT
• Acute gastric dilatation
• Erosive gastritis
• Late hypoglycemia
• Respiratory distress
• Infection (UTI)
• Hypophosphatemia
• Mucormycosis
• CVA
• Cerebral edema (rare in adults)
THANK YOU

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DIABETIC KETOACIDOSIS

• Diabetic Ketoacidosis is an acute, major, life-threatening complication

• DKA is an extreme metabolic state caused by insulin deficiency. It is

• DKA accounts for 14% of all hospital admissions of patients with

• DKA usually evolves rapidly, over a 24 hour period.

• Correction of fluid loss with intravenous fluids.

• If the initial serum potassium is below 3.3 mEq/L, IV potassium chloride

• Bicarbonate therapy is a bone of contention among physicians and still

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