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Today’s talk
Diabetes Ketoacidosis (DKA)
Hyperosmolar Non Ketotic (HONK)
Hypoglycaemia
Objectives
Recognise and participate in the management of diabetic ketoacidosis.
Recognise Hyperosmolar Non ketotic state
Recognise and manage hypoglycaemia.
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”
How would you proceed? (1)
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
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
ABG pH 7.20 pO2 16.0 pCO2 2.70 HCO3- 13.8 Na 140 K 4.3
Urinary ketones +ve
What is your differentials + why? (2)
What is your differentials + why?
Diabetes Ketoacidosis pH, blood glucose (serum), ketones
Metabolic acidosis – other causes Sepsis, poisoning
Pregnancy
Pancreatitis
Gastroenteritis
Diabetes KetoacidosisDiabetes Ketoacidosis
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
Loss of Beta cell function in pancreas
beta-cell
alpha-cell
Loss of beta cell function is gradual over time
“Honeymoon period”
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)
B L O O D
MUSCLE
Diabetic Ketoacidosis:Pathophysiolo
gy
Normal – glucose in blood
B L O O D
MUSCLEInsulin
Diabetic Ketoacidosis:Pathophysiolo
gy
Normal Mechanism
B L O O D
MUSCLE
1. Insulin deficiency
*lack of glucose in muscle
2. glucagon excess
*increase in gluconeogenesis
Diabetic Ketoacidosis:Pathophysiolo
gy
Insulin
Liver Glucagon
B L O O D
MUSCLEketones
Diabetic Ketoacidosis:Pathophysiolo
gy
3. Rapid lipolysis into free fatty acids and ketone bodies
release of Beta-hydroxybutyrate
ketones makes you sick
ketonesketones
ketones
B L O O D
MUSCLE
Diabetic Ketoacidosis:Pathophysiolo
gy
4. Hypovolaemia – vomitting + osmotic diuresis
Increases concentration of ketones + glucose
ketones
ketones
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)
How do I Manage DKA?
1. ABC – if impaired – consider early ITU input / central venous access
2. Replace fluids 3. Resolution of ketonaemia / insulin4. Replace electrolytes5. Look for cause6. Close monitoring7. Consider Low molecular weight heparin
Replacing fluidsInitial 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
Resolution of ketonaemiaInsulin infusion
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
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+ 3.5 - 5.4 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
Monitoring
Monitor urine output and vital signs closely catheterize
Repeat U&E, glucose, VENOUS bicarbonate – ABG PAINFUL
2 – 4 hours, 6 - 8 hours, 12 hours, 24 hours
Repeat ABG at 2 hours if not improving ? Alternative cause for acidosis e.g. lactate
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
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
Hyperosmolar Non-Hyperosmolar Non-Ketotic Ketotic
Hyperglycaemic State Hyperglycaemic State (HONK/HHS)(HONK/HHS)
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
B L O O D
MUSCLEInsulin
HONK:Pathophysiology
1. Insulin production markedly reduced but NOT absent.
No switch to fat metabolism and therefore no ketones or acidosis
2. Gluconeogenesis
3. Loss of intravascular volume
Importance
Mortality markedly higher compared to DKA Co-morbidities, longer time to diagnosis, electrolyte
disturbances Cerebral oedema and Pulmonary Embolism more
common
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
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
How do you calculate osmolality?
2(Na+K) + urea + glucose
Or
Ask for a serum osmolality level (U and E bottle, biochemistry)
Is the treatment the same as DKA?Is the treatment the same as 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
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
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
HypoglycaemiaHypoglycaemia
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
Causes
Drug Induced insulin sulphonylureas Alcohol
Reactive Hypoglycaemia Post prandial gastric surgery
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
Any questions about diabetic emergencies?
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.