Diabetic ketoacidosis is a life-threatening complication of diabetes caused by insufficient insulin levels. It is characterized by high blood sugar, high ketone levels, and severe acidosis. Treatment involves fluid replacement, insulin therapy to lower blood sugar, and correcting electrolyte and pH imbalances. Education on strict insulin use and management of diabetes is important to prevent future episodes of ketoacidosis.

1. DIABETIC KETOACIDOSIS
• Diabetic Ketoacidosis is an acute, major, life-threatening complication of Diabetes.
• 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.

2. PATHOPHYSIOLOGY
• It usually occurs as a consequence of absolute or relative insulin deficiency that is accompanied by an
increase in counter-regulatory hormones
insulin
counter
regulatory
hormone

4. DIAGNOSIS
DKA
KETONEMI
A
HIGH ANION
GAP
METABOLIC
ACIDOSIS
HYPERGLYCAEMI
A
ADA (American Diabetic Association -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 (Joint British Diabetes Societies- 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

5. ETIOLOGY
• Inadequate insulin treatment or noncompliance.
• New onset diabetes (20-25%)
• Acute illness
• Infection (30 to 40%)
• CVA
• Acute Myocardial Infarction
• Acute Pancreatitis
• Drugs

6. Differential diagnosis

7. 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.
SIGNS
•Confusion
• Abdominal tenderness
• 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)

9. 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!
• CXR
• ECG
• 2 D ECHO
• TROPONIN I
• USG ABDOMEN
• BLOOD / URINE
CULTURES

11. MANAGEMENT
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 OR
precipitating
factors if present.

13. 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.

14. • 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).

16. COMPLICATIONS
• CVT
• Myocardial Infarction
• DVT
• Acute gastric dilatation
• Erosive gastritis
• Late hypoglycemia
• Respiratory distress
• Infection (UTI)
• Hypophosphatemia
• Mucormycosis
• CVA
• Cerebral edema (rare in adults)

17. ADVISE ON DISCHARGE
•To not skip his insulin dose before meals
•Monitor and Maintain blood sugar levels WNL
•To modify his insulin dose on minor/ major illnesses like fever, abscess, trauma etc.
•Educate about the osmotic symptoms as marker of hyperglycemia (if blood glucose can not be
monitored at home)to maintain a brief h/o disease and treatment and kept itwith him/her
•Seek medical attention immediately

18. CLINICAL ASPECTS

19. ABG OR VBG?
•There is reasonable evidence that venous and arterial pH have sufficient agreement as to be
clinically interchangeable in patients with DKA who are hemodynamically stable and without
respiratory failure.
•Venous pH correlated well and was precise enough with arterial pH to serve as a substitute.
•ABGs can cause radial artery spasm, infarct, and/or aneurysms
•ABGs are painful to patients
•The VBG-electrolytes were 97.8% sensitive and 100% specific for the diagnosis of DKA in
hyperglycemic patient

20. TRANSITION FROM IV TO SC INSULIN
• First dose of SC insulin to be given atleast 1 hour prior to discontinuation of IV insulin infusion,
failing which allows development of rapid rebound hyperglycemia.
• Stable blood glucoses which are less than 180 mg/dL for at least 4–6 h consecutively
• Normal anion gap and resolution of acidosis in DKA.
• Stable clinical status; hemodynamic stability.
• Not on Vasopressors.
• Stable nutrition plan or patient is eating.
• Stable IV drip rates (low variability).

21. KETOSIS VS KETOACIDOSIS

22. TYPES OF KETOACIDOSIS

23. EUGLYCEMIC DKA
• It is essentially DKA without hyperglycemia (Glucose< 200).
• Euglycemic DKA is a rare entity that mostly occurs in patients with Type 1 Diabetes, but also in
Type 2 Diabetes.
• It has been associated with partial treatment of diabetes, carbohydrate food restriction,
alcohol intake, and with Sodium-Glucose Cotransporter 2 (SGLT-2) inhibitor medications
[Glifozins].
• The exact mechanism of eu DKA is not entirely known.
• Vomiting was the most common symptom.
• Management was same as DKA.

25. WHAT WE KNOW NOW?
DKA is a metabolic catastrophe due to absolute or relative insulin deficiency
Most common in type 1 diabetic patient
Diagnosed by triad of hyperglycaemia, high AG Met acidosis and ketonenemia
Fluid replacement, hyperglycaemia correction by insulin infusion, potassium and acid base
correction is the key
Look for underlying precipitating factors
Educate the pt about its pathogenesis and strict use of insulin as advised