L17 - Diabetic Emergencies

Question 1

Pathophysiology of diabetic ketoacidosis

Answer 1

Unchecked gluconeogenesis => hyperglycaemia

Osmotic diuresis => dehydration

Unchecked ketogenesis => ketosis

Dissociation of ketone bodies into hydrogen ion and anions => anion-gap metabolic acidosis

Often a precipitating event is identified (infection, lack of insulin administration)

Question 2

How does insulin deficiency lead to CV collapse?

Answer 2

Insulin deficiency => hyperglycaemia => hyperosmolality and glycosuria => dehydration and electrolyte losses

Dehydration => renal failure => shock

shock => CV COLLAPSE

Question 3

Insulin deficiency => CV collapse via LIPOLYSIS

Answer 3

Insulin deficiency => lipolysis => increased FFAs => ketones => acidosis => CV collapse

Question 4

What is the connection between to two routes to CV collapse as a result of insulin deficiency?

Answer 4

Hyperglycaemia leads to glycosuria which leads to electrolyte losses

AND ALSO

lipolysis leads to acidosis which leads to electrolyte losses

BOTH these routes lead to CV collapse

Question 5

Clinical features of diabetic ketoacidosis: age

Answer 5

mostly young T1DM

Question 6

Clinical features of diabetic ketoacidosis: precipitating causes

Answer 6

relative or absolute insulin deficiency

Question 7

Diabetic ketoacidosis - precipitating factors

Answer 7

Infections - pneumonia, urinary tract, viral illnesses, gastroenteritis

Error/missed insulin administration

MI

Previously undiagnosed T1DM

Drugs: steroids

Unidentified

Question 8

Diabetic ketoacidosis - symptoms and signs

Answer 8

Symptoms of thirst and polyuria, weakness and malaise, drowsiness, confusion caused by hyperglycaemia + dehydration

Signs of these are dry mouth, sunken eyes, postural or supine hypotension, hyperthermia and coma

Other symptoms of nausea and vomiting, abdominal pain and breathlessness are caused by acidosis

Signs of these are facial flush, hyperventilation, smell of ketones on breath and ketonuria

Question 9

Clinical features of diabetic ketoacidosis: serum sodium

Answer 9

normal or low

Question 10

Clinical features of diabetic ketoacidosis: blood glucose

Answer 10

usually <40mmol/l

Question 11

Clinical features of diabetic ketoacidosis: serum bicarbonate/pH

Answer 11

<14mmol/l / pH<7.3

Question 12

Clinical features of diabetic ketoacidosis: serum ketones

Answer 12

+++++

Question 13

Clinical features of diabetic ketoacidosis: mortality

Answer 13

5% depending on age

Question 14

Clinical features of diabetic ketoacidosis: subsequent course

Answer 14

insulin dependent

Question 15

Diabetic ketoacidosis - Management

Answer 15

5 step plan

1) Confirm diagnosis and check for precipitating causes
2) Rehydrate & monitor fluid balance
- IV fluids - saline with added potassium
- Consider urinary catheter
3) Lower glucose
- IV insulin - fixed rate 0.1Unit/kg/hr
4) Monitor electrolytes
- Potassium (and sodium)
5) Prevent clots
- Prophylactic low molecular weight heparin

Question 16

Diabetic ketoacidosis - other management factors

Answer 16

Is the patient conscious?

• Assess GCS
• If concern, call ITU

At risk of aspiration
-consider NG tube

Monitor recovery
-glucose, ketones, pH, potassium - hourly

Question 17

Diabetic ketoacidosis - recovery

Answer 17

pH normal, ketones <2+ (urine), vomiting settled

• resume normal diet
• switch from IV to normal subcutaneous insulin

Question 18

HHS stands for

Answer 18

hyperosmolar hyperglycaemic state

Question 19

Pathway of HHS

Answer 19

Insulin deficiency and glucagon adrenaline (cortisol) both cause glycogenolysis

Glycogenolysis along with increased intake of sugary drinks leads to increased hepatic glucose output and hyperglycaemia

This leads to osmotic diuresis

=> DEHYDRATION

Question 20

Hyperosmolar Hyperglycaemic State – clinical features: age

Answer 20

Usually >40years

Question 21

Hyperosmolar Hyperglycaemic State – clinical features: precipitating causes

Answer 21

Previously undiagnosed, steroids, diuretics, sugar

Question 22

Hyperosmolar Hyperglycaemic State – clinical features: serum sodium

Answer 22

Usually high

Question 23

Hyperosmolar Hyperglycaemic State – clinical features: serum bicarbonate/pH

Answer 23

Normal/ pH 7.4

Question 24

Hyperosmolar Hyperglycaemic State – clinical features: serum ketones

Answer 24

0

Question 25

Hyperosmolar Hyperglycaemic State – clinical features: mortality

Answer 25

30% (thromboses)

Question 26

Hyperosmolar Hyperglycaemic State – clinical features: subsequent course

Answer 26

Diet/tablet controlled

Question 27

HHS - Management

Answer 27

Confirm diagnosis and check for precipitating causes

Rehydrate & monitor fluid balance

• IV fluids - saline with added potassium
• Consider urinary catheter

Lower glucose (once glucose not improving with fluids)
-IV insulin - fixed rate 0.05Unit/kg/hr

Monitor electrolytes
-Potassium (and sodium)

Prevent clots
-Treatment low molecular weight heparin

Patients are often elderly and severely ill

Question 28

Causes of hypoglycaemia

Answer 28

Too little food or skip a meal; too much insulin or diabetes pills; more active than usual

Question 29

Onset of hypoglycaemia

Answer 29

Often sudden; may pass out if untreated

Question 30

Definition of hypoglycaemia

Answer 30

Hypoglycaemia is a biochemical term and exists when blood sugar < 4mmol/l but often used to describe a clinical state.

The clinical syndrome associated with hypoglycaemia develops as the nervous system becomes glucose deficient or ‘neuroglycopaenic’.

Question 31

Hypoglycaemia can be classified as:

Answer 31

asymptomatic

• awake
• sleeping

mild symptomatic (patient can treat himself)

severe symptomatic (help needed by their party)

coma and convulsions

Question 32

Autonomic symptoms of hypoglycaemia

Answer 32

Autonomic - sympathomedullary activation

sweating, feeling hot

trembling or shakiness

anxiety

palpitations

Question 33

Neuroglycopenic symptoms of hypoglycaemia

Answer 33

dizziness, light-headedness

tiredness

hunger, nausea

headache

inability to concentrate, confusion, difficulty speaking, poor coordination, behavioural change, automatism

coma and convulsions, hemiplegia

Question 34

Causes of hypoglycaemia

Answer 34

Insulin

• inappropriately excessive doses
• not eating, or insufficient carbohydrate

Sulfonylureas

Question 35

Hypoglycaemia - counter-regulation

Answer 35

Glucagon, adrenaline, cortisol and GH all have ‘anti-insulin effects’

• glucagon stimulates glycogenolysis and gluconeogenesis and is probably primary response
• adrenaline increases glycogenolysis
• GH and cortisol limit glucose disposal in peripheral tissues, but this effect takes several hours so of little benefit acutely

Sympathetic nerves may also directly activate hepatic glycogenolysis and stimulate glucagon secretion

Question 36

Hypoglycaemia - treatment

Answer 36

Minor episodes

• 20g carbohydrate as sugary drink, fruit juice, glucose tablets, glucose gels followed by something ‘starchy’ to eat
• glucose gels

Hypoglycaemic coma

• im or iv Glucagon 1mg
• iv dextrose 25g (150ml 10% glucose)