Diabetic emergencies Flashcards
What’s the most common way for new diabetes type 1 to present?
Diabetic ketoacidosis
DKA pathophysiology
Ketogenesis occurs when there is insufficient glucose supply and glycogen stores are exhausted (such as prolonged fasting):
- The liver takes fatty acids and converts them to ketones.
- Ketones are water soluble fatty acids that can be used as fuel.
- They can cross the blood brain barrier and be used by the brain as fuel
Ate ketones always harmful?
Producing ketones is normal and not harmful in healthy patients when under fasting conditions or low carbohydrate, high fat diets
What’s characteristic about the breath of people in ketosis?
ketosis = producing ketones
characteristic: acetone smell to the breath
how to measure ketones? (2)
- urinary ketones (urine dipstick)
- blood ketones (ketone meter)
What’s raised and what’s low in DKA?
- Low glucose going into the cells
- Hyperglycaemia - as glucose stays in the blood (cannot be absorbed into the cells)
Why there is dehydration and polyuria in DKA?
- The hyperglycaemia overwhelms the kidneys, and glucose starts being filtered into the urine
- The glucose in the urine draws water out with it (osmotic diuresis)
- The patient urinates a lot (polyuria)
- This results in severe dehydration
- The dehydration stimulates the thirst centre to tell the patient to drink lots of water (polydipsia)
What does the insulin normally do to the potassium?
Insulin normally drives potassium into the cell
Potassium imbalance in DKA
- Insulin normally drives potassium into cells
- Without insulin, potassium is not added and stored in cells
- Serum potassium can be high or normal (as the kidney continues to filter blood potassium)
- However, because no potassium is stored in the cells, total body potassium can be low
- When treatment with insulin starts, patients can become hypokalaemia (low serum potassium) very quickly
What’s possible K+ imbalance with insulin treatment?
treatment with insulin -> potential hypokalaemia
*this is because insulin draws potassium into the cells
What abnormalities can DKA lead to? (5)
- Hyperglycaemia
- Dehydration
- Ketosis
- Metabolic acidosis
- Potassium imbalance
Symptoms of DKA
- Polyuria
- Polydipsia
- Nausea and vomiting
- Acetone smell to their breath
- Dehydration (hypotension)
- Altered Consciousness
- They may have symptoms of an underlying trigger (i.e. sepsis)
How often and why do we need to monitor U&Es in DKA?
U&Es should be monitored extremely closely (e.g. every 2 hours) to ensure potassium remains stable
What happens in the brain cells in DKA? What’s the danger of rapid correction/ treatment of DKA?
Cerebral oedema
- Dehydration and a high blood sugar causes water to move from the intracellular space in the brain to the extracellular space
- This causes the brain cells to shrink and be dehydrated
- Rapid correction of the dehydration and hyperglycaemia (with fluids and insulin) causes a rapid shift in water from the extracellular space to the intracellular space in the brain cells
- This causes the brain to swell and become oedematous which can lead to brain cell destruction and death
How often and why do we need to do neurological observations in DKA?
- Neurological observations (including GCS) should be monitored very closely (e.g. hourly) to look for signs of developing cerebral oedema
- Be concerned in DKA patients having headaches, altered behaviour, bradycardic episodes or changes to consciousness.
Management of cerebral oedema (as complication of DKA treatment)
- slowing IV fluids
- IV mannitol
- IV hypertonic saline
Management of DKA
- fluid replacement: most patients with DKA are deplete around 5-8 litres. Isotonic saline is used initially.
- insulin: an intravenous infusion should be started at 0.1 unit/kg/hour. Once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started
- correction of hypokalaemia
- long-acting insulin should be continued, short-acting insulin should be stopped
(3) classical symptoms/signs of hyperosmolar hyperglycaemic state
Hyperglycemia result in:
- polydipsia
- electrolyte imbalance
- dehydration
Typical population profile of hyperosmolar hyperglycaemic state
type 2 elderly
*but the incidence in younger adults increase
* it may be initial presentation od diabetes type 2
Possible complications of hyperosmolar hyperglycaemic state
- vascular complications: such as myocardial infarction, stroke or peripheral arterial thrombosi
- Uncommon: Seizures, cerebral oedema and central pontine myelinolysis (CPM)
What is the difference in duration of onset between DKA and HHS?
- DKA: hours
- HHS: days (therefore as a consequence electrolyte imbalance and dehydration are more extreme)
Pathophysiology of Hyperosmolar hyperglycaemic state
- Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium
- Severe volume depletion results in a significant raised serum osmolarity resulting in hyperviscosity of blood
What is a typical picture of serum osmolarity in the hyperosmolar hyperglycaemic state?
Raised (typically > than 320 mosmol/kg)
Why a patient with HHS may not look as dehydrated as they are?
hypertonicity leads to preservation of intravascular volume
Systemic features (clinical presentation) of hyperosmolar hyperglycaemic state
- General: fatigue, lethargy, nausea and vomiting
- Neurological: altered level of consciousness, headaches, papilloedema, weakness
- Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
- Cardiovascular: dehydration, hypotension, tachycardia
hat are (3) criteria helpful in Dx of HHS (and distinguishing it from DKA)
- Hypovolaemia
- Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
- Significantly raised serum osmolarity (> 320 mosmol/kg)
3 management goals of HHS
- Normalise the osmolality (gradually)
- Replace fluid and electrolyte losses
- Normalise blood glucose (gradually)
Management of Hyperosmolar Hyperglycaemic State
- IV sodium chloride 0.9%
- Insulin (but not initially and ONLY if ketones are increased) - as we want to avoid rapid changes (rapid fall in plasma glucose)
Why insulin is not used as a 1st line in HHS?
- Fluid replacement alone with 0.9% sodium chloride solution will result in a gradual decline of blood glucose and osmolarity
- Because most patients with HHS are insulin sensitive (e.g. it usually occurs in T2DM), administration of insulin can result in a rapid decline of serum glucose and thus osmolarity.
- Insulin treatment prior to adequate fluid replacement may result in cardiovascular collapse as the water moves out of the intravascular space, with a resulting decline in intravascular volume.
What is the difference between DKA and HHS? (2)
Association:
- DKA -> T1DM
- HHS -> T2DM
Ketogenesis (ketones):
- DKA -> present
- HHS -> absent
