Diabetic ketoacidosis is a life-threatening complication of diabetes that occurs when there is not enough insulin in the body. It is characterized by high blood sugars, high ketones, and metabolic acidosis. The main treatment involves fluid replacement, insulin therapy to lower blood sugars and ketones, correcting electrolyte imbalances like potassium, and treating any underlying infections. Complications can include hypokalemia, hypoglycemia, cerebral edema, and pulmonary edema. Patient education focuses on medication adherence, sick-day management, and seeking medical care if symptoms worsen.

1. Welcome to
Morning session
By: Dr. Abdullah Al Noman
Intern doctor
Medicine dept.
TMMC&H

2. Diabetic
Ketoacidosis

3. CONTENTS
Introduction
Definition
Epidemiology
Pathophysiology
Etiology
Clinical Presentation
Laboratory Evaluation
Management
Complications
Strategies to Prevent Diabetic Ketoacidosis
Patient Counseling
References

4. INTRODUCTION
*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.

5. DEFINITION
High anion gap metabolic acidosis due
to excessive blood concentration of ketone
bodies is Ketoacidosis.
Diabetic Ketoacidosis is a state of
absolute or relative insulin deficiency
aggravated by ensuing hyperglycaemia,
dehydration & acidosis producing
derangements in intermediary metabolism.

6. EPIDEMIOLOGY
A cross-sectional study was conducted at BIRDEM General
Hospital from January 2008 to December 2011. Total
patients were 200 with:
~Female predominence - 56%
~Mean age of study population was - 37.6years
~Incidence was more in known diabetic patients
- 71%
~Low income group -76.5%
~RBS during admission was -27.1mmol/L
~In hospital mortality was -6.5%

7. PATHOPHYSIOLOGY
A- The basic underlying mechanisms are:
-Absolute deficiency of circulating insulin.
-Secretion of insulin counterregulatory
hormones: glucagon, adrenaline, cortisol and
growth hormone.

8. PATHOPHYSIOLOGY
B-This leads to disturbances in the following
physiological processes:
-glucose utilization (hyperglycemia).
- proteolysis ( amino acids, glutamine and
alanine).
- lipolysis ( glycerol and FFAs).
- glycogenolysis (breakdown of muscle glycogen
 lactate).
- gluconeogensis (glutamine & alanine & glycerol
& lactate are the precursors).

9. PATHOPHYSIOLOGY
C- This results in the following abnormalities:
1-Hyperglycemia.
2-Hyperketonemia
3-Metabolic acidosis
4-Dehydration
5-Electrolyte Imbalance

10. PATHOPHYSIOLOGY
C- This results in the following abnormalities:
1-Hyperglycemia.
2-Hyperketonemia
3-Metabolic acidosis
4-Dehydration
5-Electrolyte Imbalance

11. ETIOLOGY
Precipitating Factors:
Infections – pneumonia, UTI, sepsis, gastroenteritis
Inadequate insulin treatment or non-compliance
Infarction - Myocardial infarction, cerebral, mesenteric.
Stress
New onset diabetes
Surgery
Hyperthyroidism
Drugs – cocaine, atypical antipsychotics, corticosteroids,
glucagon, interferon
Pregnancy

12. Symptoms of DKA:
1-Classic symptoms of hyperglycemia:
Polyuria, polydipsia, wt loss and thirst.
2-Other symptoms:
- General weakness, malaise and lethargy.
-Nausea, vomiting and abdominal pain.
- Perspiration.
- Disturbed consciousness and confusion.
3-Symptoms of underlying infections or other
conditions;
-fever, abdominal pain, dysuria, chest pain.

13. Physical signs of DKA:
General signs: Ill appearance and disturbed consciousness.
Signs of dehydration:
-Skin: Dry, hot, flushed, and loss of skin turgor.
-Tongue: Dry (sometimes woody tongue).
-Eyes: Sunken eyes and dark circles under the eyes.
Vital signs:
-Tachycardia, hypotension and tachypnea.
Specific signs:
-Ketotic breath: A strong, fruity breath odour (similar to nail
polish remover or acetone).
-Acidotic breath (Kussmaul's respiration): deep and rapid.
-Abdominal tenderness.

14. Investigations
Venous blood:
Urea
Na+/ K+
Glucose
Bicarbonate
Ketones
Urine:
Ketones
Leucocyte esterase

15. Investigations
ECG
Infection screen
Full blood count
Blood and urine culture
C-reactive protein
Chest X-ray
Amylase/ lipase
Rule out Pancreatitis

16. *Hyperketonaemia (≥ 3 mmol/L) and ketonuria
(>2+ on standard urine sticks)
*Hyperglycaemia (blood glucose ≥ 11 mmol/L
(~200 mg/dL))
*Metabolic acidosis (venous bicarbonate <15
mmol/L and/or venous pH < 7.3)
Cardinal biochemical
features

17. ER Evaluation
ABC
V/S
Cardiac monitoring
Physical examination
IV access : 2 large bore lines (16-18gauge )
CVP may be needed
Blood sugar
Foley catheter

18. Diabetic Ketoacidosis
MANAGEMENT

19. Diabetic Ketoacidosis
The main lines of management include:
1. Correction of fluid loss with intravenous
fluids.
2. Correction of hyperglycemia with insulin.
3. Correction of electrolyte disturbances
particularly potassium.
4. Correction of acid-base balance.
5. Treatment of concurrent infection, if present.

20. Fluid replacement
•0.9% NaCl solution (Normal saline) i.v.
.aIf systolic BP < 90 mmHg
Give 500 mL over 10–15 mins
Repeat if SBP< 90mmHg
.bIf systolic BP ≥ 90 mmHg (for a previously well
70kg adult)
1L over 1st hour
1L over next 2 hours
1L over next 2 hours
1L over next 4 hours
1L over next 4 hours
1L over next 6 hours

21. Fluid replacement
•When blood glucose < 15 mmol/L (270
mg/dL)
• Switch to 5% dextrose, 1 L 8-hourly
• If still dehydrated, continue 0.9% saline
and add 5% dextrose, 1 L per 12 hrs
•Typical requirement is 6 L in first 24 hrs but
avoid fluid overload in elderly patients

22. Insulin Therapy
Type of insulin : Regular : Rapid or short acting insulin U-40 &
U-100.
Regimen:
Initial bolus: 0.1 U/kg body wt given IV.
Maintenance: 0.1 U/kg/body wt /hour:
IV Infusion set: Add 100 units of regular insulin +500 ml
saline i.e. every 5 cc fluid contains 1 unit of insulin
Targets:
↓ blood ketone by 0.5 mmol/L/hour
↑ bicarbonate by 3 mmol/L/hour
↓ glucose by 3 mmol/L/hour

23. Potassium Therapy
Careful monitoring of potassium is essential in Mx of DKA
because both hypo & huperkalamia may occur and potentially
life threatening.
Potassium replacement
Plasma K+> 5.5 mmol/LNil
3.5–4.5 mmol/L20 mmol/L
< 3.5 mmol/L40 mmol/L

24. 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.

25. Additional procedures:
•Catheterisation if no urine passed after 3 hrs((do it from the
start))
•Nasogastric tube to keep stomach empty in unconscious or
semiconscious patients, or if vomiting is protracted
•Central venous line if cardiovascular system compromised, to
allow fluid replacement to be adjusted accurately
•Plasma expander if systolic BP is < 90 mmHg or does not rise
with i.v. saline
•Antibiotic if infection demonstrated or suspected
•ECG monitoring in severe cases

27. Complications of DKA
1-Complications of associated illnesses e.g.
sepsis or MI.
2-Adult respiratory distress syndrome.
3-Thromboembolism (elderly).
4-Complications of treatment:
a-Hypokalemia: Which may lead to:
-Cardiac arrhythmias.
-Cardiac arrest.
-Respiratory muscle weakness.

28. Complications
b-Hypoglycemia.
c-Overhydration and acute pulmonary edema:
particularly in:
-Treating children with DKA.
-Adults with compromised renal or cardiac
function.
-Elderly with incipient CHF.

29. Complications
d-Neurological complications: Cerebral Edema.
-It occurs only in children with DKA.
-Very dangerous and increases mortality.
-The risk is related to the severity, duration and rapid
correction of DKA.
Mechanism: The brain adapts by producing intracellular osmoles
(idiogenic osmoles) which stabilize the brain cells from
shrinking while the DKA was developing. When the
hyperosmolarity is rapidly corrected, the brain becomes
hypertonic towards the extracellular fluids  water flows into
the cells  cerebral edema

30. Strategies to Prevent Diabetic
Ketoacidosis
Diabetic education
Blood glucose monitoring
Sick-day management
Home monitoring of ketones or beta-hydroxybutyrate
Supplemental short-acting insulin regimens
Easily digestible liquid diets when sick
Reducing, rather than eliminating, insulin when
patients are not eating
Guidelines for when patients should seek medical
attention
Case monitoring of high-risk patients
Special education for patients on pump management

31. Patient Counseling
Importance of medication adherence.
Proper injection technique.
Re-teach self-glucose monitoring.
Educate patient and family about
complications.
Importance of regular MD appointments.
Ways to prevent UTIs.
Q&A with patient and family.

32. References
Davidsons Principles and Practice of Medicine 22nd Edition
WWW.resarchgate.net
En.m.wikipedia.org
Joint British Diabetes Societies Inpatient Care Group guidelines
for The Management of Diabetic Ketoacidosis in Adults
British Society for Paediatric Endocrinology and Diabetes
guidelines for the management of DKA
American diabetic association guidelines

33. Diabetic Ketoacidosis