Diabetic Emergencies Flashcards

(38 cards)

1
Q

What are the 3 life-threatening diabetic emergencies?

A

Diabetic ketoacidosis (DKA)

Hyperosmolar hyperglycaemic state (HHS)

Hypoglycaemia

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2
Q

Which type of hyperglycaemic emergency is most common in type 1 and type 2 diabetes? Why is there are difference?

A

Type 1= DKA

Type 2= HHS

Difference due to type 1 having ABSOLUTE insulin deficiency whereas type 2 only has relative insulin deficiency
I.e. even small amount of insulin can act to inhibit ketogenic processes

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3
Q

What are the 4 biochemical consequences of insulin deficiency and how are they related to the symptoms of hyperglycaemic emergency?

A
  1. Increased glycogenolysis + gluconeogenesis
    - increased serum glucose leads to osmotic diuresis and consequent dehydration and loss of electrolytes (Na+ and K+)
  2. Increased proteolysis
    - increased serum AA= glucogenic and ketogenic
  3. Lipolysis
    -increased glycerol and FA= ketogenic and glucogenic
    I.e. alternative energy source due to lack of glucose uptake into cells
  4. Increased ketogenesis
    - induces metabolic acidemia i.e. ketone bodies lead to acidosis
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4
Q

What is the triad of DKA?

A

Hyperglycaemia

Ketonaemia

Metabolic acidosis

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5
Q

What are the 2 basic causes underlying the pathophysiology of DKA and why do they lead to DKA?

A
  1. Insulin deficiency
  2. Increased counter-regulatory hormones (can be released in response to stress causes by illness)

Consequences:
-increased hepatic gluconeogenesis and glycogenolysis which leads to HYPERGLYCAEMIA

-induces lipolysis which increases the concentration of free FA which induces KETOGENESIS AND KETOACIDOSIS

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6
Q

What complications of DKA can result in death?

A

Hypovolemic shock due to acidosis inducing collapse of vessels

MI

CVA

Mesenteric arterial occlusion

Acute pancreatitis

Infection i.e. pneumonia

Cerebral oedema

ARDS (pulmonary oedema)

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7
Q

What are possible precipitating factors of DKA?

A

Infection i.e. UTI or pneumonia

Treatment errors i.e. missing insulin or insufficient dose

New diagnosis of T1DM

Stress

Alcohol

Pregnancy

MI

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8
Q

What is important advice/steps that T1DM patients need to be given to help prevent DKA?

A

Sick day rules= more insulin required when unwell

Monitor blood glucose and ketones when ill

Check that pen/pump working

Don’t miss a dose (even if not eating due to illness)

Stay hydrated

Avoid strenuous activity

Keep same diet

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9
Q

What are the clinical features of DKA?

A
Hyperglycaemia:
Excessive thirst 
Polyuria 
Weight loss
Abdominal pain 
Nausea 
Blurred vision 
Ketonaemia:
Rapid breath (Acidotic respiration)
Headache 
Confusion 
Acetone breath (pear drops) 
Hot dry skin (inappropriate vasodilation)
Hypothermic (“”)
Circulatory collapse (“”) = tachycardia + hypotension 
Drowsiness 
Coma
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10
Q

Why does vasodilation occur in DKA patients and what are the clinical signs of this?

A

Acidosis induces vasodilation

Signs:

  • hot dry skin
  • hypothermic
  • circulatory collapse = hypotension and tachycardia
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11
Q

What are the 3 diagnostic criteria for DKA?

A

Glucose:
>11mmol/L or known diabetic
Lab glucose

Ketones:
Capillary blood showing ketonaemia i.e. >=3 mmol/L
Urinary test showing ketonuria i.e. >2+ on dip stick

pH:
<7.3 (venous)
HCO3 <15mmol/L

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12
Q

What other tests are important outside the diagnostic criteria and why is this?

A

Other tests can be used to assess for any precipitating factors which can them help to guide treatment

Eg:

  • U+E ie assess renal impairment to indicate level of dehydration
  • FBC and cultures= infection markers
  • ECG= evidence of MI
  • ABG to assess acid-base status= can see if acidosis has been compensated for i.e. decreased CO2
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13
Q

What happens to ureas and sodium and potassium levels in DKA and why?

A

Raised Urea= due to dehydration
Low sodium= electrolyte i.e. increased Na loss in hyperglycaemia
Low potassium= osmotic diuresis

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14
Q

What 2 forms of management should be done immediately in DKA and why?

A

Fluid replacement

  • replace circulatory volume + correct hypotension
  • clear ketones
  • correct electrolyte imbalance
Insulin = fixed rate IVII (0.1 units/kg/h)
-suppression of ketogenesis 
-reduction of blood glucose 
-correct electrolyte imbalance 
NOTE: continue normal insulin
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15
Q

What are the different things which need to be monitored in a DKA patient?

A

Blood glucose
Ketones
Blood gas for pH and HCO3
Potassium

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16
Q

What are possible complications which can arise whilst managing DKA?

A

Hypoglycaemia

Potassium derrangment

Fluid overload

17
Q

What is rebound ketosis and why does it occur? What can be done to avoid this in DKA?

A

Ketosis induced by allowing glucose levels to reach hypoglycaemic range and therefore inducing counter-regulatory hormones which induced ketosis

Give 10% glucose infusion when blood glucose falls <14mmol/L

18
Q

Why do potassium levels need to be monitored once DKA treatment has begun? When and how can it be replaced if necessary?

A

Insulin can induce fall in potassium due to activating Na+/K pump which promotes movement of K+ into cells

If fall <5.5mmol/L= 0.9% NaCl solution with potassium 40mmol/L

19
Q

How can fluid overload by managed in DKA?

A

Manage fluid balance i.e. monitor how much IV fluid going in vs how much fluid going out

Catheterise to monitor urine output

20
Q

Why might thromboprophylaxis be given in DKA? What type is given?

A

Increased risk of thromboembolism in DKA

LMWH

21
Q

What is the criteria for DKA to be classified as resolved? What are the measures taken after DKA resolution? How does this differ depending on whether px eating and drinking?

A

Blood ketone <0.3 mmol/L
Venous pH >7.3

If E+D:

  • convert to SC insulin
  • stop IVI

If not E+D:

  • move to variable rate IV insulin infusion
  • continue IVI
22
Q

What is the pathophysiology relating to HHS?

A

Hyperglycaemia causes osmotic diuresis
Osmotic diuresis causes excess water and electrolyte loss
Water moves out of intracellular compartment== cellular dehydration

23
Q

Why don’t HHS patients become ketoacidotic?

A

Insulin NOT completely absent- some present to suppress lipolysis and ketogenesis

Hyperosmolarity also inhibits lipolysis

Decreased FFA which leads to decreased induction of ketogenesis

24
Q

What are the characteristic features of patient presenting with HHS?

A

Hypovolaemia

Hyperglycaemia (>30mmol/L)

Lack of significant kyperketonaemia and acidosis

Osmolality >320 mosmol/Kg

Dehydration= 10-15% weight water deficit

Altered mental state= associated with >330mosmol/kg

Thrombotic complications

25
What are possible precipitants of HHS?
Dehydration or poor intake associate with illness Infection MI Stroke Steroids Diuretics Poor compliance with diabetes regimen or poor control
26
What is required for a diagnosis of HHS?
Serum osmolality >320 = HYPEROSMOLAR Glucose > 30mmol/L = HYPERGLYCAEMIA HCO3 >15mmol/L PH > 7.3 Blood ketones <3.0 mmol/L
27
What is the aim of HHS treatment?
Normalise osmolality Replace fluid and electrolytes Normalise BG Treat underlying causes Prevent complications i.e. A or V thrombosis/ cerebral oedema/seizures/central pontine myelinolysis
28
A patient with history of T2DM presents to A+E with increased urinary frequency, increased thirst, nausea and vomiting. What is the top differential? How can this be confirmed and how should they be managed?
HHS Serum osmolality of >320 Glucose >30mmol/L not evidence of acidosis or ketosis Managed: 1. fluid replacement: - 0.9% normal saline 2. Insulin - only if not dropping by 5mmol/L/h with saline alone - fixed rate IVII 0.05 units/kg/h 3. Potassium - only if not w/i 4-5mmol/L target with resusitation alone 4. Thromboprophylaxis (LMWH) 5. Foot protection
29
HHS patient is given fluid replacement but is not presenting with hypernatraemia. Why has this happened? How can this be avoided?
Fluid replacement gradually lowers osmolality which can cause shift in water into intracellular space Leads to increase in serum sodium== hypernatraemia Monitor osmolality and electrolytes regularly and adjust rate of saline accordingly
30
What is the difference in treatment between HHS and DKA?
Insulin NOT given as standard in HHS unless it is not falling by 5mmol/L/h
31
What is Whipple’s triad?
Symptoms of hypoglycaemia Plasma glucose conc <4mmol/L Resolution of symptoms after plasma glucose concentration raised
32
What is the biochemical definition of hypoglycaemia?
<4.0 mmol/L I.e. four= floor
33
What occurs between 3.5-3.8mmol/L glucose in hypoglycaemic patient?
Stimulates increase in counter-regulatory hormones which act to try and increase blood glucose but also contribute to the symptoms associated with hypoglycaemia Hormones: - Ad - NAd - Autonomic activity - Glucagon - GH - ADH - Cortisol
34
Symptoms associated with hypoglycaemia can fit into 2 categories? What are these categories and what are the associated symptoms? What blood glucose level do they typically present?
3.2 mmol/L Autonomic (due to increased Ad and NAd) - sweating - pallor - tachycardia - tremor - tingling - hunger Neuroglycopenic - confusion - odd behaviour - drowsiness - in coordination - slurring - diplopia - dizziness - headache
35
What are the possible causes of hypoglycaemia?
``` Excess insulin or SU Insufficient food Exercise Alcohol/drugs -impaired glucogenesis -loss of warning and can be mistaken for drunkenness Strict glycaemic control Long duration of diabetes Hypoglycaemia unawareness -elderly or children -nocturnal episodes Hot weather Renal failure ```
36
A patient presents to A+E with hypoglycaemia. They are conscious. How are they treated? How would this change if they were unconscious?
15-20g rapid acting carbohydrate Recheck BGL after 10-15 mins -repeat with carbs if still below 4 (can repeat max of 4 times) Consider 1mg IM glucagon IV glucose if still <4= 200ml of 10% over 15 mins 20g long acting carbohydrate AFTER BGL >4 + recovered Unconscious: - ABCDE - IV glucose 100ml of 20% for 15mins - 1 mg IM glucagon - recheck BGL after 10 mins and repeat IV if <4 - 20g long acting carbs after >4 + recovered
37
What are examples of 15-20g rapid acting carbs?
``` 200ml pure orange juice 4-6 glucose tablets 20g glucose gel 59ml bottle of glucose juice 150ml coke 4 jelly babies ```
38
What can be given for 20g LA carbs?
2 plain biscuits One slice of bread 200-300ml milk