Diabetes: Diabetic emergencies

Question 1

Diabetic Emergencies:

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

Answer 1

~3.6mmol/L

Question 2

Diabetic emergencies

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

Diabetic emergencies

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

Diabetic emergencies

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

Diabetic emergencies

Autonomic symptoms occurs at a glucose level of ~ [] mmol/L [1]
Name 6 symptoms

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

Answer 5

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

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

Question 6

Diabetic emergencies

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

Answer 6

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 7

Diabetic emergencies

How can you reverse hypoglycaemic unawareness? [3]

Answer 7

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 8

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

Answer 8

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

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 9

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

Answer 9

Risk of causing aspirational pneumonia

Question 10

Diabetic emergencies

If prescribing IV glucose for severe hypoglycaemia, state the ml and % glucose given over 15 mins [3]

Answer 10

• 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 11

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

Answer 11

 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 12

Patients with diabetes who wake up with which symptoms may indicate they have nocturnal hypoglycaemia? [2]

How do you confirm this diganosis? [1]

Answer 12

 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 13

Management of nocturnal hypoglycaemia? [4]

Answer 13

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

Question 14

State the triad of that defines DKA? [3]

Include numbers

Answer 14

Hyperglycemia
- Blood glucose >14 mmol/L

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

Ketosis
- Elevated serum or urine ketones

Question 15

DKA

Acidosis is caused by ketone body accumulation of which two specific ketones? [2]

Answer 15

 3-OH-butyric acid and acetoacetic acid

Question 16

DKA

DKA is terminated by administering which drug? [1]

Answer 16

 Ketosis is terminated instantaneously by insulin

Question 17

Symptomps 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

Greater severity of DKA if any of the following:

 Blood ketones > [] mmol/L
 Bicarbonate < [] mmol/L
 pH< []
 Potassium < [] mmol/L
 GCS < []
 O2 sats < []%
 Systolic BP < [] mmHg
 Pulse >[] or < [] bpm

Answer 20

 Blood ketones > 6 mmol/L
 Bicarbonate < 5 mmol/L
 pH< 7.1
 Potassium < 3.5 mmol/L
 GCS < 12
 O2 sats < 92%
 Systolic BP < 90 mmHg
 Pulse >100 or < 60 bpm

Question 21

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

Answer 21

 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 22

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 22

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 23

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 23

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 24

DKA treatment

If Ptx known to have diabetes, what is the fixed rate IV insulin infusion provided? [1]
For how long? [1]
(What happens if no response? [1]

Answer 24

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

Question 25

Most common cause of death from DKA? [1]

Answer 25

Cerebral oedema

Question 26

# Diabetic emergencies Explain the pathophysiology of **Hyperglycaemic hyperosmolar state (HHS)** [6]

Answer 26

**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 27

# Diabetic emergencies Describe the presentation of Hyperosmolar hyperglycemic state (HHS)

Answer 27

 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 28

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

Answer 28

 **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 – **perhaps 1 u/hr**

Question 29

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

Answer 29

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

Question 30

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

Answer 30

**12 hours** - then give very low doses – perhaps 1 u/hr

Question 31

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

Answer 31

Hyperglycaemic hyperosmolar state (HHS) is an acute diabetic emergency that occurs in patients with **type 2 diabetes mellitus.**

Question 32

# Diabetic emergencies HHS is characterised by which 4 presenting features? [4]

Answer 32

**Hypovolaemia** **Hyperglycaemia** (> 30 mmol/L) **Mild or absent ketonaemia** (blood ketones < 3 mmol/L) **High osmolality** (> 320 mOsm/kg)

Question 33

# DIabetic emergencies Describe the difference in onset of DKA v HHS [1]

Answer 33

**DKA** presents within **hours of onset** **HHS** comes on over **many days**