acute complication of diabetes mellitus. cardinal biochemical features for DKA. pathophysiology of DKA. clinical assesment of DKA. investigation and management for DKA. complications of DKA.

1. Acute Complication of Diabetes
Diabetic Ketoacidosis (DKA)
By : Najihah

2. • DKA is a medical emergency and remains a
serious cause of morbidity, principally in
people with type 1 diabetes.
• It has a mortality of 6-10%.
• DKA also is often the presenting problem in
newly diagnosed patient. (usually known
NIDDM patient)

3. • DKA may be precipitated by an intercurrent
illness because of failure to increase insulin to
compensate for the stress response.
- Infections (pneumonia, UTI, URI, meningitis, cholecystitis,
pancreatitis)
- Vascular disorder (MI, CVD)
- Endocrine disorders (hyperthyroidism, cushing’s, acromegaly,
pheochromocytoma)
- Trauma
- Pregnancy
- Emotional stress
- Drugs- cocaine

4. • In these conditions, there will be activation of
sympathetic stimulation which will release
epinephrine, cortisol, glucagon and growth
hormone.
• In 25% of patients, there is no precipitating
cause.

5. • Cardinal biochemical features are:
- Plasma glucose >250mg/dl
- Arterial pH <7.30
- Serum bicarbonate level <15 mEq/l
- Hyperketonemia >3mmol/L
- Ketonuria >2+ on std urine sticks

6. Pathophysiology
a. Insulin deficiency leads to hyperglycemia causes a profound
osmotic diuresis leading to dehydration and electrolyte loss.
b. Ketosis results from insulin deficiency + elevated
catecholamines and other stress hormones.
Catecholamines + Stress hormones Effects
EN , cortisol, GH Inhibit insulin mediated glucose uptake by
muscle peripheral utilization.
EN, glucagon, cortisol Activating glycogenolysis and
gluconeogenesis
EN, GH Activating lipolysis
EN, GH Inhibit residual insulin secretion

7. - These effects of inadequate insulin + catecholamines
and stress hormones lead to unrestrained lipolysis and
release FFA for hepatic ketogenesis.
- Ketogenesis produce ketone bodies in excess resulting
in ketonemia.
- This condition further depletes the electrolytes and
cause further hypovolemia.
- Underperfused tissues start producing lactic acid (due
to anaerobic metabolism).
- These along with keto-acids create a metabolic
acidosis.

8. Clinical Assesment
Symptoms :
- Polyuria, thirst - Leg cramps
- Weight loss - Blurred vision
- Weakness - Abdominal pain
- Nausea, vomitting
Signs :
- Dehydration
- Hypotension (postural/supine)
- Cold extremities/peripheral cyanosis
- Tachycardia
- Air hunger ( Kussmaul breathing )
- Smell of acetone
- Hypothermia
- Hyporeflexia ( decreased potassium )
- Confusion, drowsiness, coma (10%)

9. Investigation
• Venous blood :
- urea, electrolytes, glucose and bicarbonate (severe
acidosis plasma bicarbonate <12mmol/L)
• Urine or blood analysis for ketones.
• ECG
• Infection screen :
- CBC, blood and urine culture, C-reactive protein, chest X-ray

10. Management
1. Replacement of fluids losses.
2. Correction of hyperglycemia / metabolic
acidosis.
3. Replacement of electrolyte loss.
4. Detection and treatment of precipitating
cause.

11. 1. Replacement of fluids losses.
• Isotonic saline (0.9%) or RL solution should be used.
• The average fluid deficit in DKA is 6L (3L-
extracellular, 3L-intracellular)
• Initial fluid replacement is at a rate 5-10ml/kg/hr
over first 1-3hrs.
• In later stage, when serum sodium >155 mEq/L , 0.45%
NS may be substituted.
• Rate of infusion is reduced to 150-200ml/hr depending
on clinical status and ongoing fluid losses.

12. 2. Correction of hyperglycemia /
metabolic acidosis.
• Insulin given in a dose of 10-15 units as a bolus or
0.15 U/kg IV as an infusion is the treatment of
choice in DKA.
• Continuous infusion is given in a dose of 125
units regular insulin/250 ml NS at a rate of 0.1
unit/kg/hr.
• Insulin infusion should be given until DKA is
resolved (usually 8-24 hrs)

13. • If no suitable veins are obtainable, IM injection
can be given.
• Loading dose of 10-20 units regular insulin in
deltoid and then 5-10 units/hr q1h
- until the blood glucose concentration fall by 55-
110 mg/dL or blood ketone concentrations fall by
at least 0.5 mmol/L/hr.
• Later insulin can be given every 2-4 hours.

14. • When serum glucose lowers to 250 mg/dl, add
5% dextrose to IV solution.
• If there is presence of insulin resistance, the dose
of hourly insulin can be increased by 50-100% to
achieve proper glycemic control.
• Excessive rapid correction of hyperglycemia
(>100mg/dl/hr) has a risk of inducing osmotic
encephalopathy (especially in children).

15. 3. Replacement of electrolyte loss.
• Potassium
- Careful monitoring of potassium is essential because
both hyper and hypo can occur and are potentially
life threatening.
- Wait for serum K+ level before adding KCl to the drip.
Serum K+ Dose of KCl (mmol/l of infused fluid
>5.5 mmol/l No KCl
3.5-5.5 mmol/l 20
<3.5 mmol/l 40

16. • Bicarbonate
- Adequate fluid and insulin should resolve the
acidosis.
- It is currently not recommended
- Indications to use :
a) Life threatening hyperkalemia
b) Lactic acidosis complicating DKA
c) Severe acidosis

17. 4. Detection and treatment of
precipitating cause.
• a/microbial iv
• Reduce stress
• Hyperthyroidism
• Cessation of drugs – cocaine
• MI

18. Complications of DKA
• Metabolic
- Severe acidosis, hypokalemia, hypoglycemia,
hypocalcemia.
• Non metabolic
- Infection, septic shock, vascular thrombosis,
pulm edema, cerebral edema, lactic acidosis,
arterial thrombosis, rebound ketoacidosis
(premature cessation of insulin therapy).

19. Reference
• R Alagappan Manual of Practical Medicine ,
Fifth edition.
• Davidson’s principles and practice of
medicine, 22nd edition.
Thank You