Diabetic Ketoacidosis Hypoglycemia: DR MD Mamunul Abedin Shimul
Diabetic Ketoacidosis Hypoglycemia: DR MD Mamunul Abedin Shimul
Diabetic Ketoacidosis Hypoglycemia: DR MD Mamunul Abedin Shimul
Hypoglycemia
Dr Md Mamunul Abedin Shimul
Medical Officer
Dept of Medicine
250 bed General Hospital, Jamalpur
DKA
Diabetic ketoacidosis (DKA) is a medical emergency, principally
occurring in people with type 1 diabetes.
Mortality is higher in developing countries and among non-
hospitalized patients.
May be the presenting feature of diabetes
May be precipitated by stress, particularly infection, in those with
established diabetes. Sometimes, DKA develops because of errors in
self-management.
DKA- Cardinal Features
The cardinal biochemical features of DKA are:
Hyperketonaemia (≥ 3.0 mmol/L) or ketonuria
Hyperglycaemia (blood glucose ≥ 11mmol/L)
Metabolic acidosis (venous bicarbonate < 15 mmol/L
and/or venous pH < 7.3 (H+ > 50 nmol/L))
DKA- Pathophysiology
Hyperglycaemia causes an osmotic diuresis, leading to
dehydration and electrolyte loss.
Ketosis is caused by insulin deficiency, exacerbated by
stress hormones (e.g. catecholamines), resulting in
unrestrained lipolysis and supplying FFAs for hepatic
ketogenesis.
DKA- Pathophysiology
When ketosis exceeds the capacity to metabolise acidic
ketones, these accumulate in blood. The resulting acidosis
forces H+ ions into cells, displacing K+ ions, which are lost in
urine or through vomiting.
Patients with DKA have a total body K+ deficit but this is not
reflected by plasma K+ levels, which may initially be raised due
to disproportionate water loss.
Once insulin is started, however, plasma K+ can fall
precipitously due to dilution by IV fluids, K+ movement into
cells, and continuing renal loss of K+.
DKA- Water & Electrolyte Loss
DKA- Clinical Features
DKA- Clinical Features
DKA- Investigations
The followings are important but should not delay IV fluid and
insulin replacement:
Urea &Electrolytes,
Blood glucose,
Plasma bicarbonate (< 12 mmol/L indicates severe acidosis).
Urine and Plasma for Ketones.
ECG.
Infection screen: FBC, blood/urine culture, CRP, CXR.
DKA- Emergency management
Establish IV access, assess patient and perform initial investigations
0 – 60 Commence 0.9% Sodium Chloride:
min
-If systolic BP > 90 mmHg, give 1 L over 60 mins
-If systolic BP < 90 mmHg, give 500 mL over 10–15 mins, then
re-assess; if BP remains < 90 mmHg, repeat and seek senior review.
Commence insulin treatment:
50 U human soluble insulin in 50 mL 0.9% NaCl infused
intravenously at 0.1 U/kg body weight/hour
-Continue with SC basal insulin analogue if usually taken by
patient.
DKA- Emergency management
Perform further investigations.
0 – 60
Establish monitoring schedule:
min
-Hourly capillary blood glucose and ketone testing
-Venous bicarbonate and potassium after 1 and 2 hrs, then
every 2 hrs for first 6 hrs
-Plasma electrolytes every 4 hrs
-Clinical monitoring of O2 saturation, pulse, BP, respiratory
rate and urine output every hour
Treat any precipitating cause
DKA- Emergency management
60 mins IV infusion of 0.9% sodium chloride with potassium chloride
to added as indicated below:
06 hours 1 L over 2 hrs
1 L over 2 hrs
1 L over 4 hrs
1 L over 4 hrs
1 L over 6 hrs
Add 10% glucose 125 mL/hr IV, when glucose < 14 mmol/L
(252 mg/dL)
DKA- Emergency management
60 mins
to Be more cautious with fluid replacement in
06 hours -older or young people,
-pregnant patients and
-those with renal or heart failure;
if plasma sodium is > 155 mmol/L, 0.45% sodium chloride
may be used
DKA- Emergency management
60 mins Adjust potassium chloride infusion:
to
06 hours
DKA- Emergency management
06 to 12 Clinical status, glucose, ketonaemia and acidosis
hours should be improving; request senior review if not
Continue IV fluid replacement
Continue insulin administration
Assess for complications of treatment (fluid
overload, cerebral oedema)
Avoid hypoglycaemia
DKA- Emergency management
12 to 24 By 24 hrs, ketonaemia and acidosis should have
hours resolved (blood ketones < 0.3 mmol/L, venous
bicarbonate > 18 mmol/L)