3. Introduction of DKA
An acute and life threatening complication of
decompensated DM
More commonly with type1 DM (severe insulin
deficiency) than type2 DM
Precipitated by physiologic stress ( infection, acute
illness, missed insulin injections, CVS disease)
First presentation of undiagnosed diabetes
4. Pathophysiology of DKA
Insulin is responsible for driving glucose into
cells
When insulin is deficient, glucose can’t enter the
cells; causing hyperglycemia and cells starvation
In response to metabolic starvation, increased
level of counter-regulatory hormones (glucagon,
epinephrine, cortisol, growth hormone).
7. Clinical manifestation of DKA
Polyuria , polydipsia, dehydration
Abdominal pain
Nausea and vomiting
Altered mental status
Shock
Tachypnoea, Kussmaul’s respiration
with acetone ordor on patient’s breath
8. Investigation of DKA
Glucose in serum (hourly) and urine
Ketone in serum and urine
Serum electrolyte, BUN (2-4 hourly)
Cr ,Ca,PO4,Mg
ABGA (2-4 hourly)
Serum osmolarity
ECG for hypo/hyperkalemia
Infection screen- CP(A), CRP, blood and urine culture
CXR
9. Diagnosis features of DKA
Ketosis ( ketonaemia > 3.0 mmol/L or ketouria
>2+ on urine testing sticks)
CBG > 11.0 mmol/l and
Acidemia (bicarbonate <15 mmol/L, venous pH
< 7.3)
Serum osmolarity (<320 mOsm/L)
10. Differential diagnosis of DKA
Hyperglycemic hyperosmolar non-ketotic coma (HONK)
Starvation ketosis
Ketotic hypoglycemia
MI
Pancreatitis
Gastroenteritis
Brain stem stroke
Cerebrovascular accident
11. Differential diagnosis of DKA
High anion gap metabolic acidosis
Alcoholic ketoacidosis
Ethylene glycol/methanol poisoning
Lactic acidosis
Salicylate poisoning
Uremic acidosis
Rhabdomyolysis
12. Complication of DKA
Hypotension, Shock
Hypoglycemia
Hypophosphatemic muscle weakness during
recovery from DKA
Acute tubular necrosis from severe dehydration
Hemolysis, Myoglobinuria due to acidosis
Pulmonary oedmea and ARDS secondary to fluid
overload
13. Complication of DKA
CVS complication - Arrhythmias
CNS complication
vascular thrombosis ( secondary to dehydration
and hypercoagulability )
Cerebral oedema
14. Management of DKA
Include correcting Hypovolemia, hyperglycemia, total
body potassium deficit and prompt treatment of
precipitating causes.
Continuous infusion of isotonic fluids with K+ and
insulin infusion
Multidisciplinary management with involvement of
senior surgeons, anaesthetists, diabetologists and
intensivists are essential.
15. Initial assessment
Confirmation of Dx and rapid assessment of ABCD
100% oxygen , FM with RB
In patients with reduced conscious or coma(GCS <8),
consider intubation and ventilation
16. Fluid therapy
Total water deficit – 6L
Initially, 0.9% Normal Saline 1-2L for the first hour,
followed by 200-500ml/hr to correct dehydration
Goal- to replace half of water and sodium deficit
over 12-24 hours.
In patients with hypotension, continue until BP is
stable
17. Insulin Therapy
FRII with 0.1 unit/kg/hr, it reduces 50-60% of
sugar in 1st 4hrs (Goal- ↓ 100mg/dl/hr or 10%/hr)
If resistant, infusion rate may be increased.
Reduce insulin infusion rate 0.02-0.05 unit/kg/hr
when glucose <12mmol/l
FRII continues until pH>7.3, HCO3 >15mmol/L,
and blood ketone <0.6mmol/L
18. Electrolyte Therapy
(1) Potassium
K+ replacement is initiated when K+ <5.3 mmol/L
20-30mmol of K+ to each Liter of infused fluid
In severe hypokalemia, K+ <3.3 mmol/L, replacement
at 10-20mmol/hr should commence immediately with
fluid therapy
Only initiate insulin when K+> 3.3mmol/L
19. Electrolyte Therapy
(2) Bicarbonate
Controversial
pH between 6.9 and 7.1, no risk or benefit
When pH<6.9 to partially correct acidosis
100 mmol sodium bicarbonate in 400 ml of isotonic solution
with 20 mmol KCl, 200 ml/h for two hours until venous pH>7
Life threatening hyperkalaemia is indication for bicarbonate
therapy
20. Electrolyte Therapy
(3) Phosphate
Routine phosphate replacement not beneficial
Correction of severely low levels (<0.4 mmol/L) may be
necessary (muscle weakness, impaired cardiac systolic
performance and haemolytic anaemia)
Excessive replacement >> hypocalcemia , calcium should
be monitored.
21. Electrolyte Therapy
(4) Magnesium
Benefit not demonstrated in DKA
Principles of magnesium supplementation similar
to other critical care situation
22. Management of DKA
stop IV insulin,
IV fluids
start SC insulin
0.5-0.8 unit/kg.
Blood glucose < 200-250 mg/dl
HCO3 ≥ 15 mEq/L
pH>7.3
anion gap <12 mEq/L
23. Management of DKA
Antibiotics if infection is present
Prophylactic unfractionated or LMWH until
mobile, no dehydration or elevated serum
osmolality
NG drainage to prevent aspiration
Urinary catheterisation for strict fluid balance
Continuous ECG monitoring
Notes recording
24. Take home message
DKA is acute and life threatening
Triad of Hyperglycemia, ketosis and acidosis
Fluid, IV insulin and correction of electrolyte
imbalance with frequent monitoring is essential.
Identifying and treating the precipitating cause
Early detection and prompt treatment of
complications
