Tutorial 8 - Diabetic Ketoacidosis Flashcards
(17 cards)
What factors can precipitate diabetic ketoacidosis?
- No cause
- No insulin
- New diagnosis
- Ischaemic event
- Infection
- Other
What happens in insulin deficiency?
- High HGP (Hepatic Glucose Production)
- Deficient muscle glucose uptake
What happens when there’s a high plasma glucose concentration to the kidney?
Glucose exceeds the proximal convoluted tubule’s ability for reabsorption when plasma glucose concentration is too high.
Glycosuria ensues
Why can hyperglycaemia cause dehydration?
See picture attached
What happens to fatty acids in the liver when plasma insulin concentration is low?
Fatty acids are used to produce ketone bodies in the liver and not glucose
Where are ketones produced in insulin deficiency?
In the liver
How can ketosis result from hyperglycaemia?
See attached picture
Why is there loss of muscle mass in T1DM?
Lots of glycogen leaves the muscle
List some facts about the distal convoluted tubule
- Needs adequate glomerular filtration for the acid base system to function
- Carbonate dehydratase is important in acid base homeostasis
- Na excretion is linked to H or K excretion
- Acid ketone bodies require increased HCO3 buffering
What form of acidosis ensues as a result of diabetic ketoacidosis?
Metabolic acidosis
- low pH
- low HCO3
- due to impaired production
- also due to increased H+ buffering
- low CO2
What are the clinical features of diabetic ketoacidosis?
- Dehydration
- Polyuria and polydipsia due to osmotic diuresis
- Hyperventilation (Kussmaul)
- Insulin deficiency
- Total body potassium deficiency, although plasma [potassium] high
- Glycosuria
- Ketonuria
- Acidotic
- Abdominal pain, vomiting
- Coma
- Risk of arrhythmia, infection and dilated stomach
What investigations would you do for diabetic ketoacidosis?
- Capillary glucose
- Plasma glucose
- Creatinine, K+, Na+
- FBC
- Arterial blood gases
- Amylase (triglyceride)
- ECG
- CXR
- Septic screen
What is the treatment for diabetic ketoacidosis?
Fluid
- Normal Saline
- H2O 100ml/kg
- Na+ 8mmol/kg
- 3-8L in 24 hours
- Do not replace whole deficit too quickly
Insulin
- Given as an I.V. sliding scale
- Capillary glucose is measured once an hour
- Insulin administration rate is adjusted according to that measurement
- Insulin should not be stopped, even if the plasma glucose appears low
Potassium
- Normally plasma potassium is 4-5mmol/l
- Even after treatment, is rare that a patient develop hyperkaelaemia unless they have severe renal disease
- 6mmol/l >>> give non and check
- 5mmol/l >>> 10mmol/hr
- 4mmol/l >>> 20mmol/hr
- 3mmol/l >>> 25mmol/hr
- <3 large K+and recheck
Bicarbonate
Other measures
- Cardiac monitor - arrythmias
- Catheterise
- Antibiotics
- NG tube (gastroparesis)
- Consider heparin
- Consider arterial line (very acidotic) and central line (elderly or when cardiac failure)
What is the risk/benefit of bicarbonate treatment?
DANGER OF BICARBONATE
- Negativeinotropism
- Peripheral vasodilation
- Hypotension
- Cerebral inhibition
DANGER OF ACIDAEMIA (DANGER OF NO BICARBONATE)
- Hypokalaemia
- Hypernatraemia
- REbound alkalosis
- CSF acidosis
- Impaired oxyHb dissociation
After initial diabetic ketoacidosis treatment, what is involved in the second phase of management?
When glucose < 10mmol / litrechange to 5% dextrose
Continue insulin
Continue potassium
May need more saline
What are the causes of death in diabetic ketoacidosis?
- Self-neglect
- Social factors
- Delay seeking heko
- Delay in primary care
- Inappropriate treatment
- Overwhelming disease
How can diabetic ketoacidosis be prevented?
- Education
- Never stop insulin
- Check glucose and modify insulin if ill
- Admit if vomiting
