Diabetes: Diabetic emergencies

Question 1

Diabetic patients typically starting presenting with symptoms when their hypoglycaemia gets to what mmol/L gluocse? [1]

Answer 1

~3.6mmol/L

Question 2

Describe what is meant by ‘false hypoglycaemia’ [1]

Answer 2

patients with consistently high glucose levels may experience symptoms of hypoglycaemia at a higher level than someone with good glycaemic control

Question 3

Name 4 non medical causes of hypoglycaemia [4]

Answer 3

 Exercise with too much insulin or not enough carbs
 Alcohol – can cause hypoglycaemia even in non-diabetic people
 Vomiting
 Breastfeeding

Question 4

State 4 medical causes of hypoglycaemia [4]

Answer 4

 Liver disease
 Progressive renal impairment
 Hypoadrenalism (is associated with Type 1 diabetes)
 Hypothyroidism
 Hypopituitarism (rare)
 Insulinoma (rare)

Question 5

Autonomic symptoms occurs at a glucose level of ~ [] mmol/L [1]

Name 6 symptoms

Answer 5

Autonomic symptoms – Glucose ~ 3.6 mmol/L
 Sweating
 Shaking or tremor
 Anxiety
 Palpitations
 Hunger Nausea

Question 6

Neuroglycopenic symptoms occurs at a glucose level of ~ [] mmol/L [1]
Name 5 symptoms

Answer 6

Neuroglycopenic symptoms– Glucose ~ 2.7 mmol/L
 Confusion
 Drowsiness
 Slurred speech
 Aggression
 Visual disturbances

Question 7

Describe the phenomenon of hypoglycaemic unawareness [1]
State 3 causes [3]

Answer 7

Loss of early warning signs of hypoglycaemia (25% of people with Type 1 diabetes may be unable to recognise)
Causes:
 Increased duration of diabetes
 Very tight glycaemic control
 Autonomic neuropathy

Question 8

How can you reverse hypoglycaemic unawareness? [3]

Answer 8

May be improved by “hypo holiday”:
 Strict hypoglycaemia avoidance by relaxing glycaemic control
 Use of analogue insulin
 Continuous Subcutaneous Insulin Infusion (insulin pump therapy)

Question 9

Treatment of mild [2], moderate [2] and severe [4] hypoglycaemia?

Answer 9

Mild:
 Sugary drink, e.g. lucozade, ordinary coke, orange juice
 5-7 glucose tablets, or 3-4 heaped teaspoons of sugar in water

Moderate:
 Glucogel® – 1-2 tubes buccally (into cheek), or jam, honey, treacle massaged into the cheek.
 Intramuscular glucagon if needed

Severe (unconscious)
 Do not put anything in the mouth
 Place the person in the recovery position Administer 0.5-1mg glucagon IM
 If carer is unable to administer glucagon, call 999
 In hospital, administer iv glucose:
- Ideally 75mls of 20% glucose or 150mls 10% glucose over 15 mins
- 50mls 50% glucose can be given, but take care with veins – extravasation can cause chemical burns

Question 10

What is the dose of IV glucose for hypoglycaemia? [2]

Answer 10

75mls of 20% glucose or 150mls 10% glucose over 15 mins

Question 11

Name a risk of giving glucogel orally? (For moderate hypoglycaemia) [1]

Answer 11

Risk of causing aspirational pneumonia

Question 12

Post hypo once glucose above 4.0 mmol/L, must have give patients what? [1]

Answer 12

Carbs:
 Two biscuits
 One slice of bread/toast
 200-300ml glass of milk (not soya)
 Normal meal if it is due (but must contain carbohydrate)

Question 13

Patients with diabetes who wake up with which symptoms may indicate they have nocturnal hypoglycaemia? [2]
How do you confirm this diganosis? [1]

Answer 13

 High blood glucose levels (rebound hyperglycaemia)
 Headaches – feels “hungover” despite no alcohol!

 Confirm by advising testing blood glucose levels during the night (3.00am), or using continuous glucose monitoring sensor (CGMS), which monitors glucose over 5 days subcutaneously

Question 14

Management of nocturnal hypoglycaemia? [4]

Answer 14

 Analogue insulins
 Pre bed snack
 Change timing of insulin
 Insulin pump therapy

Question 15

State the triad of that defines DKA? [3]
(Include values)

Answer 15

Hyperglycemia
- Blood glucose >14 mmol/L

Acidosis
- pH < 7.30
- Bicarb< 15 mmol/L

Ketosis
- Elevated serum or urine ketones

Question 16

DKA is terminated by administering which drug? [1]

Answer 16

Ketosis is terminated instantaneously by insulin

Question 17

Symptoms of DKA? [5]

Answer 17

Often a short history:

 Abdominal pain and vomiting is common – can present as an acute abdomen
 Kussmaul’s respiration – deep sighing respirations due to acidosis
 Ketones on breath (remember ~40% people cannot smell these)
 Drowsiness, confusion
 Dehydration and Tachycardia

Question 18

State 5 triggers of DKA [5]

Answer 18

 Insulin omission (see notes later on “sick day rules”)
 Infection
 Pregnancy
 Myocardial Infarction
 Intoxication / drugs

Question 19

Diagnosis of DKA?
Venous blood gases [2]
CBG [1]
Ketones? [1]

Answer 19

 Venous blood gases:
- show acidosis (pH < 7.35, bicarb < 15)

 Capillary Blood Glucose (CBG)
- usually over 14 mmol/L, but can be lower (euglycaemic ketosis or alcoholic ketosis)

 Raised Urea and Creatinine
 Urine or plasma ketones
- elevated: above 3 mmol/L

Question 20

What supportive management and monitoring would Ptx with DKA be provided with? [5]

Answer 20

 Level 2 bed (High Dependency Unit)
 Cardiac monitor
 Nasogastric tube if impaired conscious level
 Consider Central Venous Pressure line – especially in elderly
 Oxygen if PaO2 < 10.5 kPa on air
 Urinary catheter
 Prophylactic LMW heparin
 iv antibiotics as appropriate if suspected infection
 Frequent monitoring of conscious level, BP, Pulse, Temp, Glucose, Urine output, Potassium, Acidosis

Question 21

What are the main goals of management in a patient presenting with DKA? [5]

Answer 21

Restore circulating volume and tissue perfusion
Clear serum/urinary ketones and halt ketogenesis
Decrease serum glucose towards a normal level
Correct electrolyte derangements
Identify and treat underlying precipitant

Question 22

Describe the overall management plan for DKA

Answer 22

1. Fluid therapy: 0.9% NaCl; 5/10% glucose at a rate of 125 ml/hour (when serum glucose is below 14 mmHg
2. IV Insulin therapy: 0.1 units/kg/hr
3. Monitor Electrolytes: Insulin treatment will decrease plasma potassium levels leading to profound hypokalaemia.

Question 23

Describe fluid therapy provided for DKA patients:

Sodium chloride:
- What %? [1]
- How many litres, over what time period? [4]

Glucose:
- What %? [1]
- What level CBG mmol/L is required before giving? [1]
- How much ml/hr? [1]

Answer 23

Sodium chloride 0.9%
* 1 Litre stat
* 1 Litre in 1 hour
* 1 Litre over 2 hours (+20 mmol potassium chloride) 1 Litre over 4 hours (+potassium chloride)
* 1 Litre over 4 hours (+potassium chloride)

5% or 10% Glucose
* Start when the CBG is < 12 mmol/L and continue at 125ml/hr
* 10 % glucose may be necessary to increase insulin infusion Increase infusion rate if glucose falls below 6.0 mmol/L`

Question 24

When is potassium provided in DKA fluid therapy? [1]
What levels of K are provided for patients with serum K of:
* < 3.5 [1]
* 3.5-5.5 [1]
* > 5.5 [1]

Answer 24

For the first 1-2 bags fluid, give no potassium as fluid is given too rapidly

For every subsequent bag of NaCl 0.9% or glucose 5% use a bag of fluid containing KCl as follows according to serum K+:
- < 3.5: May need additional K+ and delay insulin
- 3.5-5.5: 20-40 mmol/l
- > 5.5: none

Question 25

what is the fixed rate IV insulin infusion provided for DKA? [1]
For how long? [1]
(What happens if no response?

Answer 25

0.1 u /kg – around 6-8 u / hr for most patients
If not achieved – increase rate by 1 u / hr

Question 26

Most common cause of death from DKA? [1]

Answer 26

Cerebral oedema

Question 27

The serum potassium concentration should be maintained between [] and [] mmol/L in DKA patients.

Answer 27

The serum potassium concentration should be maintained between 4.0 and 5.5 mmol/L.

Question 28

What levels of ketones, venous pH and bicarbonate would indicate patient has returned to normal after DKA? [3]

Answer 28

ketones: is less than 0.6 mmol/L,
venous pH over 7.3
and/or venous bicarbonate over 18 mmol/L.

Question 29

What effect does insulin have on K levels? [1]

Answer 29

intravenous insulin regime, which will decrease plasma potassium levels leading to profound hypokalaemi (causes intracellular movement of K)

Question 30

Describe the issues regarding K levels during DKA [2]

Answer 30

Severe dehydration & insulin deficiency can lead to pre-renal acute kidney injury and transmembrane shifts in potassium due to the ketoacidosis.

These collectively lead to hyperkalaemia.

However, on initiation of insulin therapy plasma potassium concentrations dramatically fall leading to dangerous hypokalaemia.

Question 31

Explain the pathophysiology of Hyperglycaemic hyperosmolar state (HHS) [6]

Answer 31

Relative lack of insulin is coupled with a rise in counter-regulatory hormones (e.g. cortisol, growth hormone, glucagon) that leads to a profound rise in glucose.

These patients retain a certain level of insulin, which prevents the development of ketosis that epitomises DKA. However, the level of insulin is inadequate to prevent profound hyperglycaemia.

The excessive glucose leads to massive osmotic diuresis within the kidneys with the loss of essential electrolytes such as sodium and potassium.

This is because the proximal tubules within the kidneys only have a certain capacity for reabsorption of glucose. Once this is reached, the remaining glucose is passed through the renal nephrons causing diuresis

As water is lost, there is profound dehydration and reduced circulating volume, resulting in hyperosmolarity and marked hyperglycaemia. Patients with HHS may have up to a 9 litre deficit of water

The increase in osmolality increases compensatory mechanisms such as release of anti-diuretic hormone (ADH) and stimulation of thirst. However, if this cannot compensate for the renal water loss (e.g. elderly patients with co-morbidities) then hypovolaemia develops with progression to acute kidney injury, electrolyte disturbances, hypotension and coma.

The hyperosmolar state of the condition leads to hyperviscosity that increases the risk of arterial and venous thrombosis (e.g. stroke, DVT).

Question 32

Describe the presentation of Hyperosmolar hyperglycemic state (HHS) [4]

Answer 32

 Usually Type 2 diabetes
 Longer subacute history
 Hyperglycaemia often >40 mmol/L
 NOT ketoacidotic, but may have lactic acidosis
 Severe dehydration
 Patient is often hypernatraemic

Question 33

What are the treatments for Hyperosmolar hyperglycemic state (HHS)? [2]

Answer 33

 Due to the significant fluid deficit, the initial management requires fluid resuscitation to restore circulating volume:
- 0.9% NaCl and at least 1 litre should be given over an hour (quicker in the presence of significant hypotension).
- Fluid replacement alone with 0.9% sodium chloride solution will result in falling blood glucose
- Further fluids can be given aiming for a positive fluid balance based on hourly measurement of urine output. A proposed target is 2-3 litres positive by 6 hours.

 Insulin:
- IVI as for DKA – but consider slower fluids if elderly / heart failure
- much lower dose insulin – (maybe) no insulin for 1st 12 hours, then very low doses : rate of 0.05 units/kg/hour if blood ketones (beta-hydroxybutyrate) are ≤3.0 mmol/L and the patient is not acidotic

Question 34

Why is fluid therapy given slowly when treating HHS? [1]

Answer 34

Rapid correction of the fluid deficit is not advisable as it can precipitate osmolar shifts leading to cerebral oedema (generally aim for 4 litres positive within the first 24 hour).

Question 35

What K should be given for the following serum K levels when treating HHS & DKA?

Serum K+ > 5.5 mmol/L: [1]
Serum K+ 3.5-5.5 mmol/L: [1]
Serum K+ < 3.5 mmol/L: [1]

Answer 35

Serum K+ > 5.5 mmol/L: Nil potassium replacement
Serum K+ 3.5-5.5 mmol/L: 40 mmol potassium replacement
Serum K+ < 3.5 mmol/L: Senior review for more invasive potassium replacement

Question 36

What pathology is a risk of rapid shift of glucose in HHS patient treatment? [1]
Why? [1]

Answer 36

 Rapid shifts in glucose should be avoided due to risk of rapid fluid / sodium shifts, and risk of central pontine myelinolysis (CPM)

Question 37

How long do you not give insulin for HHS treatment? [1]

Why? [1]

Answer 37

12hrs

Insulin treatment prior to adequate fluid replacement may result in cardiovascular collapse
as water moves out of the intravascular space, with a resulting decline in intravascular volume

Question 38

Hyperglycaemic hyperosmolar state (HHS) is an acute diabetic emergency that occurs in patients with type [] diabetes mellitus.

Answer 38

DMT2

Question 39

Which other electrolytes are common to have a deficiency in HHS? [2]

Answer 39

Hypophosphataemia and hypomagnesaemia are common in HHS.

Question 40

All patients should receive [] for the full duration of HHS admission unless contraindicated

Explain why [1]

Answer 40

All patients should receive prophylactic low molecular weight heparin (LMWH) for the full duration of admission unless contraindicated

Higher risk of VTE: (DM is a risk factor; hospitilisation; hypovolaemia)