Diabetic Ketoacidosis Acute Management: A State of Absolute Insulin Bankruptcy
Diabetic Ketoacidosis Acute Management: A State of Absolute Insulin Bankruptcy
Diabetic Ketoacidosis Acute Management: A State of Absolute Insulin Bankruptcy
Acute management
missed therapy
Surgery
Diagnostic criteria
• Elderly
• Pregnant ladies
• Heart or kidney failure
• Other serious comorbidities
• Severe DKA by following criteria:
– Venous bicarbonate <5 mmol/L
– Blood ketones >6 mmol/L
– Venous pH <7.1
– Hypokalaemia on admission (<3.5 mmol/L)
– Glasgow Coma Scale (GCS) <12
– Oxygen saturation <92% on air (arterial blood gases required)
– Systolic BP <90 mm Hg
– Pulse >100 or <60 beats/minute
– Anion gap >16
Anion Gap = (Na+ K) – (Cl + HCO3-)
Management
FLuid loss Electrolytes
Hyperglycemia Acidosis
Precipitating
Factor
1st Hour: Immediate Management
Step 1. Commence 0.9% NS drip using large bore cannula.
Step 2. Commence a fixed rate (0.1 unit/kg/hr based on estimate of weight).
intravenous insulin infusion (IVII) 1U/mls short-acting human insulin in 0.9% NS solution.
Step 3. Assess patient • BP, Pulse, Temperature, Respiratory rate, Oxygen saturation
• Glasgow Coma Scale
• Hydration status
• Full clinical examination
Step 4 • Capillary and venous blood glucose
Investigations • Arterial blood gases
• Blood or urinary ketones
• BUSE, FBC
• Blood cultures, MSU
• ECG (if indicated)
• CXR (if indicated)
Step 5 Hourly capillary blood glucose
Outline monitoring regimen • VS and IO charting hourly
• HCO3 and K level at 60 minutes,
4 hours and 6-hourly thereafter
• 6-hourly BUSE and urine ketone
• Continuous SpO2 (if indicated)
• Continuous cardiac monitoring (if indicated)
Step 6. Look for precipitating Start broad-spectrum antibiotics if infection suspected
causes and treat accordingly
use with caution
Fluids commencement
Potassium replacement
HCO3
• Avoid hypoglycaemia
Step 12. Reassess patient, monitor vital signs, review biochemical and
metabolic parameters
• At 12 hours check venous pH, bicarbonate, potassium, capillary ketones
and glucose
• If not resolved review Step 9 and Step 10.
If DKA resolved go below
Resolution of DKA
Expectation:
Patient should be eating and drinking and back on normal insulin
• If DKA is not resolved identify and treat the reasons for failure to
respond
• Convert to subcutaneous regime when biochemically stable (blood
ketones <0.3 mmol/L, pH >7.3) and the patient is ready and
able to eat.
http://www.cmft.nhs.uk/media/383957/dka%20guidelines%20-%202012.pdf
Additional reading
https://emcrit.org/pulmcrit/blood-gas-measurements-dka-searching-unicorn/
• obesity itself causes some degree of insulin resistance. Patients who are not obese
by traditional weight criteria may have an increased percentage of body fat distributed
predominantly in the abdominal region. Ketoacidosis seldom occurs spontaneously in
this type of diabetes; when seen, it usually arises in association with the stress of
another illness such as infection. This form of diabetes frequently goes undiagnosed
for many years because the hyperglycemia develops gradually and at earlier stages
is often not severe enough for the patient to notice any of the classic symptoms of
diabetes. Nevertheless, such patients are at increased risk of developing
macrovascular and microvascular complications. Whereas patients with this form of
diabetes may have insulin levels that appear normal or elevated, the higher blood
glucose levels in these diabetic patients would be expected to result in even higher
insulin values had their β-cell function been normal. Thus, insulin secretion is
defective in these patients and insufficient to compensate for insulin resistance.
Insulin resistance may improve with weight reduction and/or pharmacological
treatment of hyperglycemia but is seldom restored to normal. The risk of developing
this form of diabetes increases with age, obesity, and lack of physical activity. It
occurs more frequently in women with prior GDM and in individuals with hypertension
or dyslipidemia, and its frequency varies in different racial/ethnic subgroups. It is often
associated with a strong genetic predisposition, more so than is the autoimmune form
of type 1 diabetes. However, the genetics of this form of diabetes are complex and
not clearly defined.
acetoacetate vs 3-beta-hydroxybutyrate
• CONCLUSIONS:
There is reasonable evidence that venous and arterial pH have
sufficient agreement as to be clinically interchangeable in patients with
DKA who are haemodynamically stable and without respiratory failure.
There is some evidence that venous and arterial bicarbonate also
agree closely in DKA