L17 - Acute complications diabetes

Question 1

Diabetic ketoacidosis - patho

Answer 1

osmotic diuresis - dehydration
unchecked gluconeogenesis - hyperglycemia
unchecked ketogenesis - ketosis
Dissociation of ketone bodies into hydrogen ion and anions - Anion-gap metabolic acidosis

Question 2

How is acidosis managed?

Answer 2

intracellular buffering H+/K+ exchange

respiratory compensation - hyperventilation

renal excretion of H+ ions

Question 3

What are precipitating factors in diabetic keto?

Answer 3

infections - pneumonia/viral
error/missed insulin administration
myocardial infarction
drugs - steroid

Question 4

diabetic ketoacidosis signs and symptoms

Answer 4

thirst polyuria - sign dry mouth, sunken eyes, postural hypotension
Nausea vomiting - facial flush, hyperventilation

Question 5

clinical features of diabetic ketoacidosis

Answer 5

age - mostly young in t1d
precipitating causes - insulin deficiency
serum sodium - normal or low
blood glucose - usually less than 40 mmol/l
serum bicarbonate less than 14mmol/l and pH less than 7.3
serum ketones +++++
mortality 5% depending ona age
subsequent course: insulin dependent

Question 6

5 step plan for managing diabetic ketoacidosis?

Answer 6

1 - confirm diagnosis and check for precipitating causes
2 - rehydrate and monitor fluid balance. iv fluids saline with added potassium consider a urinary catheter
3 - lower glucose - iv insulin
4 - monitor electrolytes - potassium and sodium
5 - prevent clots - prophylactic low molecular weight heparin

Question 7

Other management factors for DKA?

Answer 7

is the patient conscious? assess GCS
At risk of aspiration - consider NG tube
monitor recovery - glucose, ketones, pH, potassium - hourly

Question 8

DKA recovery

Answer 8

pH normal
ketones less than 2+(urine)
vomiting settled 
resume normal diet 
switch from IV to normal subcutaneous insulin

Question 9

what is Hyperosmolar Hyperglycaemic State (HHS)

Answer 9

Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis.
Patient has got insulin, so there is no fat breakdown but not enough insulin to stop glucose getting higher and higher so pee the glucose out leading to dehydration
commonly in old and frail patients who dont drink enough water

Question 10

HSS age

Answer 10

usually 40+

Question 11

preciptating causes for HSS

Answer 11

previously undiagnosed, steroids, diuretics, sugar

Question 12

serum sodium HSS

Answer 12

Usually high

Question 13

blood glucose HSS

Answer 13

Often more than 40 mmol/l

Question 14

serum bicarbonate and pH in HSS

Answer 14

Bicarbonate - normal

pH - 7.4

Question 15

serum ketones in HSS

Answer 15

0

Question 16

Subsequent course HSS

Answer 16

Diet/tablet controlled

Question 17

HSS management

Answer 17

correct the profound dehydration

Question 18

What is hypoglycemia?

Answer 18

Hypoglycaemia is a biochemical term and exists when blood sugar < 4mmol/l but is often used to describe a clinical state. The clinical syndrome associated with hypoglycaemia develops as the nervous system becomes glucose deficient or ‘neuroglycopaenic

Question 19

Symptoms of hypoglycaemia

Answer 19

Autonomic – sympathomedullary activation
Sweating, feeling hot
Trembling or shakiness
Anxiety
palpitations
Neuroglycopenic
Dizziness, light-headedness
Tiredness
Hunger, nausea
Headache
Inability to concentrate, confusion, difficulty speaking, poor coordination, behavioural change, automatism
Coma and convulsions, hemiplegia

Question 20

Hypoglycemia causes

Answer 20

insulin - inappropriately excessive doses
not eating/insufficient carbohydrate
sulfonylureas

Question 21

how can you counter regulate hypoglycemia?

Answer 21

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 22

Hypoglycemia treatment

Answer 22

Minor episodes: 20g carbohydrate as sugary drink, fruit juice, glucose tablet
glucose gel

Hypoglycemic coma -
IM or IV glucagon 1mg
IV dextrose 25g

Question 23

mild/moderate hypo treatment

Answer 23

patient conscious and able to swallow
give 5 level teaspoons glucose powder in water
or 120mls lucozade or 5 glucose tablets
test blood glucose after 15 minutes
if less than 4 mmol/l repeat up to 3 times
if more than 3 times, consider 1mg glucagon IM
then long acting carbohydrate - 2 biscuits or a slice of bread

Question 24

severe hypo treatment

Answer 24

patient unconscious or nil by mouth or very aggressive
check ABC stop any IV insulin
if pt suitable for IM glucagon give 1mg.
if not give 10% IV glucose 150 ml repeat up to 3 times
recheck glucose levels after 15 mins. long acting carb
If NBM give 10% glucose infusion at 100ml/hr until no longer NBM