Diabetic Metabolic Emergencies Flashcards
Give examples of diabetic metabolic emergencies.
Diabetic Ketoacidosis (DKA)
Hyperosmolar hyperglycaemic state
Lactic acidosis
Mortality rate of DKA.
Around 1%
Why does DKA occur?
In which type of diabetes?
Marked insulin deficiency.
T1DM
When does DKA usually occur?
Previously undiagnosed diabetes
Interupption of insulin therapy
Stress of intercurrent illness and infection
What is the most common error leading to DKA?
To reduce or omit insulin because the individual feels unable to eat owing to nausea or vomiting.
Although insulin adjustments are necessary they should never be stopped.
Definition of Ketonuria.
Detectable ketone levels in the urine.
Occurs after fasting in people without diabetes.
Also found in people with relatively well-controlled T1DM as well.
Definition of ketosis.
Elevated plasma ketone levels in the absence of acidosis.
Definition of DKA.
Metabolic emergency where hyperglycaemia is associated with a metabolic acidosis due to greatly raised ketone levels.
Ketone levels in DKA.
>3 mmol/l
Define hyperosmolar hyperglycaemic state.
Metabolic emergency in which uncontrolled hyperglcyaemia induces a hyperosmolar state in the absence of significant ketosis.
Define lactic acidosis.
Metabolic emergency in which elevated lactic acid levels induce a metabolic acidosis.
Associated with metformin therapy.
Pathogenesis of DKA.
Marked insulin deficiency leads to elevated counter-regulatory hormones such as glucagon.
The insulin deficiency leads to hyperglycaemia secondary to increased gluconeogenesis, and diminished insulin mediated peripheral glucose uptake.
This leads to osmotic diuresis, profound dehydration and loss of electrolytes.
More importantly there is uncontrolled lipolysis in adipose tissue and uncontrolled ketogenesis in the liver.
Usually only very little insulin is required to inhibit ketogenesis and adipose TAG breakdown.
The body will start to use the ketone bodies as an alternative fuel and they build up because of impaired uptake into peripheral tissues.
This leads to acidosis.
Explain the acidosis in DKA.
Ketone bodies are nauseating and many people will vomit.
This leads to worsening dehydration and further electrolyte loss.
Along with ketone bodies contributing to the acidosis the plasma osmolality will rise and the renal perfusion will fall. This impairs renal excretion of hydrogen ions and ketones, making the acidosis even worse.
Clinical features of DKA.
Prostration
Dehydration
Nausea
Vomiting
Abdominal pain
Some might be mentally alert, some may not be.
Hyperventilation (Kussmaul respiration)
Smell of ketones
Confirmation of diagnosis of DKA.
Ketonaemia >3 mmol/l or significant ketonuria >2
Blood glucose > 11 mmol/l or known diabetes
Bicarbonate below 15 mmol/l and/or venous pH <7.3
Blood potassium levels should also be assessed.
Potassium levels in DKA.
Metabolic acidosis causes hyperkalaemia as potassium is exchanged for hydrogen ions moving into the cell.
Insulin promotes the co-transport of potassium along with glucose into cells as well which counteracts the hyperkalaemia.
However even if serum potassium is elevated there is a severe whole-body potassium deficiency as significant quantities of potassium are lost in vomit and urine.
Indicators of severe DKA.
Blood ketones over 6 mmol/l
Bicarbonat < 5 mmol/l
Venous/arterial pH below 7.0
Hypokalaemia on admission
GCS less than 12
O2 sat below 92% on air
SBP below 90 mmHg
Pulse over 100 or below 60
Anion gap above 16.
What are the immediate (0-60 minutes) measures of DKA.
Assess the severity.
Initial investigations like blood ketones, capillary and venous glucose, serum creatinine and electrolytes, venous blood gases, FBC, cultures, ECH, CXR + cardiac monitoring.
A - IV infusion with 0.9% sodium chloride to counteract the dehydration. This is given 1 L over first hour unless there is hypotension and they require more rapid.
B - Add 40 mmol/L of potassium if the potassium is < 5.5 mmol/l.
C - Fixed rate of IV insulin infusion at a rate of 0.1 unit/kg per hour. This is by using human insulin.
D - Continue long-acting basal insulin at the usual dose and time.
In short -
Severity -> Investigations -> IV fluids -> Potassium (if needed) -> insulin
Management of DKA from 60 min to 6 hours.
- *A -** Reassessment of patient. Consider urinary catheterisation if patient is incontinent or anuric after 2h - 4h.
- *Consider nasogastric tube** insertion if patient is persistently vomiting.
B - Continue IV fluids (0.9% saline with potassium chloride)
C - Measure blood ketones and capillary glucose hourly.
D - Measure venous blood gas for pH, bicarbonate and potassium at 60 minutes and hourly thereafter.
E - Identify and treat precipitating factors.
What should the levels of ketones be as they are measured hourly from 60 minutes to 6h.
What else can be measured?
Measure blood ketones to make sure they fall by at least 0.5 mmol/l per hour. If not increase insulin infusion rate by 1.0 per hour.
Can also measure venous bicarbonate which should rise by 3.0 mmol/l per hour.
Can also measure glucose that should fall by at least 3.0 mmol/l per hour.
Management from 6h to 12h of DKA.
Reassess the patient and review biochemical and metabolic measurement to check for resolution of DKA.
When is conversion to subcutaneous insulin appropriate?
When they are biochemically stable
This means blood ketones less than 0.6 mmol/l
pH > 7.3
Ready and able to eat.
Why should potassium not be prescribed with the initial fluid resuscitation?
Because there is a risk of acute pre-renal kidney injury associated with severe dehydration .
What is hyperchloraemic acidosis?
An acidosis that may develop during treatment of DKA since there is a large variety of negatively charged electrolytes that are lost and replace with chloride.
This is usually corrected by the kidneys spontaneously within a few days.
Why should bicarbonates generally not be given for DKA?
Because it can lead to development of cerebral oedema and may cause a paradoxical increase in CSF acidosis.
It is only used if the pH is < 7.0.
Why should a nasogastric tube be considered if the patient keeps vomiting?
Because aspiration of vomit can be fatal.
What can the dehydration, increased blood viscosity and coagulability in DKA lead to?
Fatal thromboembolism.
Thromboprophylaxis with LMWH heparin should be considered.
Complications of DKA.
Cerebral oedema (rare)
Severe hypothermia.
What is hyperosmolar hyperglycaemic state?
When severe hyperglycaemia develops without significant ketosis.
It is a metabolic emergency of uncontrolled T2DM.
Which people present with HHS?
People in middle or later life.
Often with previously undiagnosed diabetes.
Common precipitating factors of HHS.
Consumption of glucose-rich fluids
Concurrent medication like thiazides or steroids
Intercurrent illness
The main differences between DKA and HHS.
Age - Old people experience thirst less acutely and become dehydrated more readily. The mild renal impairment associated with age results in increased urinary losses of fluid and electrolytes. This leads to increased osmolality.
The insulin deficiency is less severe in HHS compared to DKA. Endogenous insulin levels are enough to inhibit hepatic ketogenesis however not sufficient enough to inhibit hepatic glucose production.
Gluconeogenesis occurs, ketogenesis does not.
Anion gap in DKA vs HHS
E.g. DKA = 40
HHS = 25
Characteristic clinical features of HHS.
Dehydration
Stupor
Coma
Impaired consciousness related to degree of hyperosmolality
What might the hyperosmolar state predispose?
Stroke
MI
Lower limb arterial insufficiency
Investigation of HHS.
Similar to keto-acidosis.
Check plasma osmolality by measuring it directly or calculated as (2(Na+ + K+) + glucose + urea).
Management of HHS.
Fluid replacement with 0.9% saline.
If osmolality is not declining adequately 0.45% saline can be considered.
What should the rate of fall of plasma sodium not exceed?
Why?
10 mmol/l in 24 hours
Because the correctional change of osmolality may result in cerebral damage.
Fluid replacement is often enough to lower the glucose.
If the glucose is not falling with fluids alone, what can be given?
Insulin at 0.05 units/kg per hour.
This is also given if the patient develops significant ketonaemia.
What should the rate of fall of blood glucose not exceed?
Why?
Should not be more than 5 mmol/l per hour.
To prevent cerebral damage.
What should be given prophylactically when treating HHS?
LMWH to prevent the predisposition to stroke, MI and lower limb arterial insufficiency.
Mortality of HHS.
15-20%
Mainly because of the advanced age of patients compared to in DKA and also the frequent intercurrent illness.
Insulin need in DKA vs HHS.
HHS is not an absolute indication for subsequent insulin therapy, compared to ketoacidosis.
Treatment of lactic acidosis in diabetes.
Rehydration and infusion of isotonic 1.26% bicarbonate.
Mortiliaty is in excess of 50%.
Stop metformin
