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

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diabetes emergencies

Diabetes Emergencies

Christian Hariman

Christian.hariman@uhcw.nhs.uk

today s talk
Today’s talk
  • Diabetes Ketoacidosis (DKA)
  • Hyperosmolar Non Ketotic (HONK)
  • Hypoglycaemia
objectives
Objectives
  • Recognise and participate in the management of diabetic ketoacidosis.
  • Recognise Hyperosmolar Non ketotic state
  • Recognise and manage hypoglycaemia.
case rose smith
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
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
slide7

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
slide8

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
What is your differentials + why?
  • Diabetes Ketoacidosis
    • pH, blood glucose (serum), ketones
  • Metabolic acidosis – other causes
    • Sepsis, poisoning
  • Pregnancy
  • Pancreatitis
  • Gastroenteritis
who gets dka
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
Loss of Beta cell function in pancreas

Loss of beta cell function is gradual over time

“Honeymoon period”

alpha-cell

beta-cell

symptoms and signs
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)
diabetic ketoacidosis pathophysiology

MUSCLE

Diabetic Ketoacidosis:Pathophysiology

Normal – glucose in blood

B L O O D

diabetic ketoacidosis pathophysiology17

MUSCLE

Diabetic Ketoacidosis:Pathophysiology

Normal Mechanism

B L O O D

Insulin

diabetic ketoacidosis pathophysiology18

Liver

Glucagon

MUSCLE

Diabetic Ketoacidosis:Pathophysiology
  • Insulin deficiency
  • *lack of glucose in muscle
  • glucagon excess
  • *increase in gluconeogenesis

B L O O D

Insulin

diabetic ketoacidosis pathophysiology19

MUSCLE

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

ketones

ketones

diabetic ketoacidosis pathophysiology20

MUSCLE

Diabetic Ketoacidosis:Pathophysiology

4. Hypovolaemia – vomitting + osmotic diuresis

Increases concentration of ketones + glucose

ketones

B L O O D

ketones

how do i diagnose dka
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
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
replacing fluids
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
resolution of ketonaemia insulin infusion
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
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
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
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 acidosisif 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
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
honk hyperosmolar hyperglycaemic state 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
honk pathophysiology

MUSCLE

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

Insulin

importance
Importance
  • Mortality markedly higher compared to DKA
    • Co-morbidities, longer time to diagnosis, electrolyte disturbances
    • Cerebral oedema and Pulmonary Embolism more common
clinical presentation
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 to30%
  • 2/3 cases previously undiagnosed
  • As high as 50% mortality
how do i recognise it
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
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?
  • 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
insulin
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
hypoglycaemia40
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
Causes
  • Drug Induced
    • insulin
    • sulphonylureas
    • Alcohol
  • Reactive Hypoglycaemia
    • Post prandial
    • gastric surgery
treatment of hypoglycaemia
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

summary
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.
  • Christian.Hariman@uhcw.nhs.uk