1. Christian Hariman Christian.hariman@uhcw.nhs.uk
Diabetes Emergencies
Christian Hariman

2. Today’s talk Diabetes Ketoacidosis (DKA)
Hyperosmolar Non Ketotic (HONK)
Hypoglycaemia

3. Objectives
Recognise and participate in the management of diabetic ketoacidosis.
Recognise Hyperosmolar Non ketotic state
Recognise and manage hypoglycaemia.

4. Case – Rose Smith 18 year old girl, known diabetic type 1
Brought in by her parents as she had been sick
Recently split from her boyfriend 2 days ago
Has been vomiting all night
She had been drinking alcohol with her mates yesterday to “cheer her up”

5. How would you proceed? (1)

6. How would you proceed? ABC of resuscitation History + examination
Pregnancy check?
Blood tests – FBC, U+E, LFTs, CRP, amylase
Blood glucose
Arterial blood gas
Urinary ketones

7. A - patent
B - 29 breaths per minute, rapid shallow breaths, 100% on air
C – BP 102/68. Pulse 107. Cap refill 7 sec
History – as above
Examination – slightly tender abdomen
Pregnancy check –ve
Bloods taken
Peripheral blood glucose 9.0

8. ABG Urinary ketones +ve pH 7.20 pO2 16.0 pCO2 2.70 HCO3- 13.8 Na 140

9. What is your differentials + why? (2)

10. What is your differentials + why?
Diabetes Ketoacidosis
pH, blood glucose (serum), ketones
Metabolic acidosis – other causes
Sepsis, poisoning
Pregnancy
Pancreatitis
Gastroenteritis

11. Diabetes Ketoacidosis

12. Who gets DKA? Hallmark of type 1 diabetes (insulin insufficiency)
Previously undiagnosed DM (about 25 – 30%)
Interruption to normal insulin regime
Intercurrent illness - usually infection

13. Loss of Beta cell function in pancreas
Loss of beta cell function is gradual over time
“Honeymoon period”
alpha-cell
beta-cell

14. Symptoms and signs Nausea Vomiting Abdominal pain
Often preceding polyuria, polydipsia, weight loss
Drowsiness/confusion/coma (severe)
Kussmaul respiration - hyperventilation
‘Pear drops’ breath
Sign of associated systemic illness (MI, infection, etc)

16. Diabetic Ketoacidosis:Pathophysiology
Normal – glucose in blood
B L O O D
MUSCLE

17. Diabetic Ketoacidosis:Pathophysiology
Normal Mechanism
B L O O D
MUSCLE
Insulin

18. Diabetic Ketoacidosis:Pathophysiology
Liver
Glucagon
Insulin deficiency
*lack of glucose in muscle
glucagon excess
*increase in gluconeogenesis
B L O O D
MUSCLE
Insulin

19. Diabetic Ketoacidosis:Pathophysiology
3. Rapid lipolysis into free fatty acids and ketone bodies
release of Beta-hydroxybutyrate
ketones makes you sick
B L O O D
ketones
ketones
MUSCLE
ketones
ketones

20. Diabetic Ketoacidosis:Pathophysiology
4. Hypovolaemia – vomitting + osmotic diuresis
Increases concentration of ketones + glucose
ketones
B L O O D
MUSCLE
ketones

21. How do I diagnose DKA? Diagnosis requires all 3 of the following:
High blood sugar (i.e diabetes) Glucose > 11 mmol
*Finger-prick blood glucose can be normal*
Ketones (blood or urine ≥ +++)
Acidosis (pH<7.30 or HCO3<15mmol)

22. How do I Manage DKA?
ABC – if impaired – consider early ITU input / central venous access
Replace fluids
Resolution of ketonaemia / insulin
Replace electrolytes
Look for cause
Close monitoring
Consider Low molecular weight heparin

23. Replacing fluids Initial management 1L 0.9% NaCl
30 mins*
1hr
2hr
4 hr
Then continue NaCl 0.9% as dictated by fluid status
*beware of elderly patients
Later
Once blood glucose <14 mmol/L – give 10% dextrose alongside 0.9% Normal Saline at 125ml / hour
Colloid initially if hypotensive
Don’t switch NaCl to 5% dextrose alone - results in swinging results

24. Resolution of ketonaemia Insulin infusion
50units actrapid made to 50ml with NaCl 0.9%
Rate: 0.1 units/kg/hour
70kg = 7 units/hour
Aim for fall in serum ketone of 0.5 mmol/L per hour
OR rise in serum HCO3- by 3 mmol/hr or reduction of Blood glucose by 3 mmol/hr
Increase rate of insulin by 1 unit per hour if above not achieved
Continue infusion until blood ketones <0.3, venous pH >7.3 and/or HCO3- >18

25. Replace electrolytes K+ is most important
Insulin shifts K+ into cells therefore K+ will fall as rehydrate
Serum K+ ≥ 5.5
No potassium supplement
Serum K
Add 20mmol per litre
Serum K+ <3.5
Add 40mmol per litre
Hyponatraemia may occur due to osmotic effect of glucose - it will correct with treatment of DKA

26. Monitoring Monitor urine output and vital signs closely
catheterize
Repeat U&E, glucose, VENOUS bicarbonate – ABG PAINFUL
2 – 4 hours, hours, 12 hours, 24 hours
Repeat ABG at 2 hours if not improving
? Alternative cause for acidosis e.g. lactate

27. Pitfalls Does a high wcc mean infection?
No, not necessarily!
Give antibiotics as guided by findings
Absence of fever doesn’t mean absence of infection
Consider alternative cause for acidosis if glucose and acidosis markedly out of proportion
Non specific abdo pain and raised amylase doesn’t always mean pancreatitis
Do not stop insulin even if the blood glucose is normal or below 4

28. Discharge, Prognosis and Prevention
How do you stop a sliding scale?
Overlap with normal insulin (breakfast) and keep in for an other 24 hours to monitor BMs
Prevention
Diabetic nurse + docs can use opportunity for patient education about insulin regime etc.
Mortality is < 5%
Patients with frequent episodes are at increased risk of dying and diabetic complications

29. Hyperosmolar Non-Ketotic Hyperglycaemic State (HONK/HHS)

30. HONK: Hyperosmolar hyperglycaemic state (HHS)
Hallmark of type 2 DM
May occur in:
New diagnosis
Poor compliance with treatment
Intercurrent illness – especially MI, Infection, CVA
Drugs- Steroids
Sugary drinks

32. HONK:Pathophysiology
Insulin production markedly reduced but NOT absent.
No switch to fat metabolism and therefore no ketones or acidosis
Gluconeogenesis
Loss of intravascular volume
B L O O D
MUSCLE
Insulin

33. Importance Mortality markedly higher compared to DKA
Co-morbidities, longer time to diagnosis, electrolyte disturbances
Cerebral oedema and Pulmonary Embolism more common

34. Clinical Presentation
Possibly osmotic symptoms
Dehydration around 10L deficit
Decreased level of conciousness
Signs of underlying infection in up to 50%
+/- thrombo-embolism in up to 30%
2/3 cases previously undiagnosed
As high as 50% mortality

35. How do I recognise it? Diagnosis requires ALL of the following:
Raised blood glucose (usually >30mmol)
Absence of ketones (or + or ++ only)
Serum osmolality >350mmol

36. How do you calculate osmolality?
2(Na+K) + urea + glucose Or
Ask for a serum osmolality level (U and E bottle, biochemistry)

37. Is the treatment the same as DKA?
1L 0.9% NaCl
1 hr*
2 hr
4 hr
8 hr
Then continue NaCl 0.9% as dictated by fluid status
*half the rate of DKA
Fluid replacement – SLOWER (may be a marker of population not pathology)
Electrolyte replacement (pseudohyponatraemia)
Insulin – ‘slower’ scale – normally very responsive to IV insulin
Search for cause
ANTICOAGULATION
Monitor

38. Insulin 50units actrapid made to 50ml with NaCl 0.9%
Rate: 0.1 units/kg/hour
70kg = 7 units/hour
More insulin sensitive
Reduce rate if Blood glucose falls >10 mmol / hour
Consider halving the rate within the first 1-2 hours
Stop when patient is recovered

39. Hypoglycaemia

40. Hypoglycaemia In diabetes: blood sugar < 4 mmol/l
Symptoms may not present at the same level of blood glucose
Autonomic:
sweating, palpitations, tremor, hunger
Neuroglycopenic
confusion, clumsiness, behavioural changes, seizures
Non-specific
nausea, headache, tiredness

41. Causes Drug Induced insulin sulphonylureas Alcohol
Reactive Hypoglycaemia
Post prandial
gastric surgery

42. Treatment of hypoglycaemia
If able to eat
glucose: e.g 3 dextrosol tabs / 200mls of orange juice/ coca cola
followed by long acting carbohydrate eg toast/ sandwich
In the community: 1mg glucagon im and long acting carbohydrate on recovery
Hospital options-
I.M. glucagon 1mg
I.V. 20ml of 50% dextrose*
Other: hypostop
*Extravasation of 50% dextrose can cause severe tissue loss; 20% preferable

43. Any questions about diabetic emergencies?

44. Summary You should be able to: Recognise diabetic ketoacidosis.
Participate in the management of diabetic ketoacidosis.
Recognise Hyperosmolar Non ketotic state
Recognise and manage hypoglycaemia.