Diabetic Metabolic Emergencies

Question 1

Give examples of diabetic metabolic emergencies.

Answer 1

Diabetic Ketoacidosis (DKA)

Hyperosmolar hyperglycaemic state

Lactic acidosis

Question 2

Mortality rate of DKA.

Answer 2

Around 1%

Question 3

Why does DKA occur?

In which type of diabetes?

Answer 3

Marked insulin deficiency.

T1DM

Question 4

When does DKA usually occur?

Answer 4

Previously undiagnosed diabetes

Interupption of insulin therapy

Stress of intercurrent illness and infection

Question 5

What is the most common error leading to DKA?

Answer 5

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.

Question 6

Definition of Ketonuria.

Answer 6

Detectable ketone levels in the urine.

Occurs after fasting in people without diabetes.

Also found in people with relatively well-controlled T1DM as well.

Question 7

Definition of ketosis.

Answer 7

Elevated plasma ketone levels in the absence of acidosis.

Question 8

Definition of DKA.

Answer 8

Metabolic emergency where hyperglycaemia is associated with a metabolic acidosis due to greatly raised ketone levels.

Question 9

Ketone levels in DKA.

Answer 9

>3 mmol/l

Question 10

Define hyperosmolar hyperglycaemic state.

Answer 10

Metabolic emergency in which uncontrolled hyperglcyaemia induces a hyperosmolar state in the absence of significant ketosis.

Question 11

Define lactic acidosis.

Answer 11

Metabolic emergency in which elevated lactic acid levels induce a metabolic acidosis.

Associated with metformin therapy.

Question 12

Pathogenesis of DKA.

Answer 12

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.

Question 13

Explain the acidosis in DKA.

Answer 13

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.

Question 14

Clinical features of DKA.

Answer 14

Prostration

Dehydration

Nausea

Vomiting

Abdominal pain

Some might be mentally alert, some may not be.

Hyperventilation (Kussmaul respiration)

Smell of ketones

Question 15

Confirmation of diagnosis of DKA.

Answer 15

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.

Question 16

Potassium levels in DKA.

Answer 16

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.

Question 17

Indicators of severe DKA.

Answer 17

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.

Question 18

What are the immediate (0-60 minutes) measures of DKA.

Answer 18

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

Question 19

Management of DKA from 60 min to 6 hours.

Answer 19

• *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.

Question 20

What should the levels of ketones be as they are measured hourly from 60 minutes to 6h.

What else can be measured?

Answer 20

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.

Question 21

Management from 6h to 12h of DKA.

Answer 21

Reassess the patient and review biochemical and metabolic measurement to check for resolution of DKA.

Question 22

When is conversion to subcutaneous insulin appropriate?

Answer 22

When they are biochemically stable

This means blood ketones less than 0.6 mmol/l

pH > 7.3

Ready and able to eat.

Question 23

Why should potassium not be prescribed with the initial fluid resuscitation?

Answer 23

Because there is a risk of acute pre-renal kidney injury associated with severe dehydration .

Question 24

What is hyperchloraemic acidosis?

Answer 24

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.

Question 25

Why should bicarbonates generally not be given for DKA?

Answer 25

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.

Question 26

Why should a nasogastric tube be considered if the patient keeps vomiting?

Answer 26

Because aspiration of vomit can be fatal.

Question 27

What can the dehydration, increased blood viscosity and coagulability in DKA lead to?

Answer 27

Fatal thromboembolism.

Thromboprophylaxis with LMWH heparin should be considered.

Question 28

Complications of DKA.

Answer 28

Cerebral oedema (rare)

Severe hypothermia.

Question 29

What is hyperosmolar hyperglycaemic state?

Answer 29

When severe hyperglycaemia develops without significant ketosis.

It is a metabolic emergency of uncontrolled T2DM.

Question 30

Which people present with HHS?

Answer 30

People in middle or later life.

Often with previously undiagnosed diabetes.

Question 31

Common precipitating factors of HHS.

Answer 31

Consumption of glucose-rich fluids

Concurrent medication like thiazides or steroids

Intercurrent illness

Question 32

The main differences between DKA and HHS.

Answer 32

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.

Question 33

Answer 33

Question 34

Anion gap in DKA vs HHS

Answer 34

E.g. DKA = 40

HHS = 25

Question 35

Characteristic clinical features of HHS.

Answer 35

Dehydration

Stupor

Coma

Impaired consciousness related to degree of hyperosmolality

Question 36

What might the hyperosmolar state predispose?

Answer 36

Stroke

MI

Lower limb arterial insufficiency

Question 37

Investigation of HHS.

Answer 37

Similar to keto-acidosis.

Check plasma osmolality by measuring it directly or calculated as (2(Na+ + K+) + glucose + urea).

Question 38

Management of HHS.

Answer 38

Fluid replacement with 0.9% saline.

If osmolality is not declining adequately 0.45% saline can be considered.

Question 39

What should the rate of fall of plasma sodium not exceed?

Why?

Answer 39

10 mmol/l in 24 hours

Because the correctional change of osmolality may result in cerebral damage.

Question 40

Fluid replacement is often enough to lower the glucose.

If the glucose is not falling with fluids alone, what can be given?

Answer 40

Insulin at 0.05 units/kg per hour.

This is also given if the patient develops significant ketonaemia.

Question 41

What should the rate of fall of blood glucose not exceed?

Why?

Answer 41

Should not be more than 5 mmol/l per hour.

To prevent cerebral damage.

Question 42

What should be given prophylactically when treating HHS?

Answer 42

LMWH to prevent the predisposition to stroke, MI and lower limb arterial insufficiency.

Question 43

Mortality of HHS.

Answer 43

15-20%

Mainly because of the advanced age of patients compared to in DKA and also the frequent intercurrent illness.

Question 44

Insulin need in DKA vs HHS.

Answer 44

HHS is not an absolute indication for subsequent insulin therapy, compared to ketoacidosis.

Question 45

Treatment of lactic acidosis in diabetes.

Answer 45

Rehydration and infusion of isotonic 1.26% bicarbonate.

Mortiliaty is in excess of 50%.

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