Acute Complication of Diabetes Mellitus: Laksmi Sasiarini
Acute Complication of Diabetes Mellitus: Laksmi Sasiarini
Acute Complication of Diabetes Mellitus: Laksmi Sasiarini
of
Diabetes Mellitus
Laksmi Sasiarini
Hyperglycemic Crisis
Diabetic Ketoacidosis (DKA)
Hyperosmolar hyperglycemic state (HHS)
Hypoglycemia
Second edition
Update September 2013
Laboratory findings
Differential diagnosis
History of polyuria, polydipsia, weight loss,
dehydration, weakness, and mental status change.
PRECIPITATING FACTOR(S)
Fluid administration and deficits
0.45% NaCl (250 – 500 ml/h) depending 0.9% NaCl (250 – 500 ml/h)
on hydration state depending on hydration state
Insulin has several effects, but the following are the most important when treating
DKA :
• Suppression of ketogenesis
• Reduction of blood glucose
• Correction of electrolyte disturbance
Initial serum Initial serum Initial serum
K+< 3.3 mEq/L K+ ≥ 5.0 mEq/L K+ 3.3 – 5.5 mEq/L
Hold insulin and give 20- Do not give K+ and Give 20 – 30 mEq K+ in
30 mEq K+/h until K+ > check K+ every 2 h each liter of iv fluid (2/3
3.3 mEq/L as KCL and 1/3 as
KPO4) to keep serum
K+ at 4 – 5 mEq/LmEq
pH < 6.9 pH ≥ 6.9
Check electrolyte, BUN, venous pH, creatinine and glucose every 2 – 4 hours until
stable
After resolution of DKA or HHS and when patient is able to eat, initiate SC
multidose insulin regimen.
To transfer from IV to SC, continue IV indulin infusion for 1-2 hr after SC insulin
begun to ensure adequate plasma insulin levels.
In insulin naïve pts, start at 0.5 U/kg to 0.8 U/kg body weight per day and adjust
insulin as needed.
Continue to look for precipitating factor(s).
Resolution of DKA is defined as
pH > 7.3 units;
bicarbonate > 15.0mmol/L; and
blood ketone level < 0.6mmol/L
(rather than < 0.3mmol/L),
The ADA Workgroup on Hypoglycemia defined
hypoglycemia in diabetes as “all episodes of abnormally
low plasma glucose concentration that expose the
individual to potential harm ”.
50
Patients affected per year (%)
40
30
20
10
0
Sulphonylurea- Insulin- “Standard” insulin Intensively
treated type 2 treated type 2 therapy in type 1 Treated in type 1
diabetes diabetes diabetes diabetes (DCCT)
Excessive Error by patient, doctor or pharmacist
dosage
HYPOGLYCEMIA
HYPOGLYCEMIA
• Neuroglycopenic
AUTONOMIC
When the blood glucose levels drop significantly, the body releases
epinephrine. This triggers certain processes like releasing the glucose
stored in the liver (glycogen) in an attempt to stabilize the blood glucose
levels.
Epinephrine also affects the nervous system and results in these
characteristic signs and symptoms :
Anxiety
Dizziness
Hunger
Palpitations
Sweating
Trembling
These symptoms are the early warning signs but may be absent in certain
cases. In patients who experience frequent episodes of hypoglycemia, the
body may stop releasing epinephrine. This is known as hypoglycemic-
associated autonomic failure (HAAF) or is also referred to as hypoglycemia
unawareness. The blood glucose levels continue to drop until the
neuroglycopenic symptoms may be evident. It may only be at this point
that the appropriate measures are implemented.
NEUROGLYCOPENIC
As the blood glucose levels continue to drop without any
intervention, the glucose supply to the brain is severely
impaired and may result in the symptoms listed below.
Blurred vision
Confusion
Difficulty concentrating
Drowsiness
Irritability, anger
Poor coordination
Speech difficulty
Autonomic Neuroglycopenic Malaise
Sweating Confusion Nausea
Pounding heart Drawsiness Headache
Tremor Speech difficulty
Hunger Incoordination
Atypical behaviour
Visual disturbance
Circumoral paraesthesia
+
+
ACTH
+
100
Altered symtoms of hypoglycaemia
Relationships
between the 50
duration of
diabetes (a) 0
100
Sweating and/or tremor
(b) 0
100
Severe hypoglycaemia without warning
50
0
(c) 0-9 10-19 20-29 30-39 > 40
Duration of diabetes (years)
Established
Capillary blood sample
diagnosis
Evaluation
Intramuscular glucagon
0.5 – 1 mg Repeat
after 10 ‘
Maintainance
180 – 200 mg% Intravenous glucose 20
10% Dextrose – 30 ml 50% dextrose
Dexamethasone
Principal metabolic effects of counter-regulation
in response to acute hypoglycaemia