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.
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.
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.
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
Notes de l'éditeur
Insulin resistance = failure of blood glucose to fall w/in 1 hr
Osmotic encephalopathy = cerebral edema, it is fatal.
