Diabetes: Diabetic emergencies Flashcards

 Be able to distinguish between the following terms and conditions: hypoglycaemia; diabetic ketoacidosis; hyperglycaemia; hyperosmolar hyperglycaemic state  Know how to manage a hypoglycaemic patient  Know how to manage a patient with diabetic ketoacidosis  Know how to manage a patient in a hyperosmolar hyperglycaemic state  Understand the precipitating factors in hyperglycaemic states

1
Q

Diabetic Emergencies:

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

A

~3.6mmol/L

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2
Q

Diabetic emergencies

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

A

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

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3
Q

Diabetic emergencies

Name 4 non medical causes of hypoglycaemia [4]

A

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

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4
Q

Diabetic emergencies

State 4 medical causes of hypoglycaemia [4]

A

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

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5
Q

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

A

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

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6
Q

Diabetic emergencies

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

A

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

:

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7
Q

Diabetic emergencies

How can you reverse hypoglycaemic unawareness? [3]

A

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

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8
Q

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

A

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

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9
Q

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

A

Risk of causing aspirational pneumonia

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10
Q

Diabetic emergencies

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

A
  • 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
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11
Q

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

A

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

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12
Q

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

How do you confirm this diganosis? [1]

A

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

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13
Q

Management of nocturnal hypoglycaemia? [4]

A

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

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14
Q

State the triad of that defines DKA? [3]

Include numbers

A

Hyperglycemia
- Blood glucose >14 mmol/L

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

Ketosis
- Elevated serum or urine ketones

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15
Q

DKA

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

A

3-OH-butyric acid and acetoacetic acid

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16
Q

DKA

DKA is terminated by administering which drug? [1]

A

 Ketosis is terminated instantaneously by insulin

17
Q

Symptomps of DKA? [5]

A

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

18
Q

State 5 triggers of DKA [5]

A

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

19
Q

Diagnosis of DKA?:

Venous blood gases [2]
CBG [1]
Ketones? [1]

A

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)

20
Q

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

A

 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

21
Q

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

A

 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

22
Q

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]

A

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

23
Q

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]

A

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

24
Q

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]

A

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

25
Q

Most common cause of death from DKA? [1]

A

Cerebral oedema

26
Q

Diabetic emergencies

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

A

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).

27
Q

Diabetic emergencies

Describe the presentation of Hyperosmolar hyperglycemic state (HHS)

A

 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

28
Q

Diabetic emergencies

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

A

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

29
Q

Diabetic emergencies

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

A

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

30
Q

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

A

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

31
Q

Diabetic emergencies

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

A

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

32
Q

Diabetic emergencies

HHS is characterised by which 4 presenting features? [4]

A

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

33
Q

DIabetic emergencies

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

A

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