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

transcript

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

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

Normal – glucose in blood

B L O O D

MUSCLEInsulin

Normal Mechanism

B L O O D

MUSCLE

1. Insulin deficiency

*lack of glucose in muscle

2. glucagon excess

*increase in gluconeogenesis

Insulin

Liver Glucagon

B L O O D

MUSCLEketones

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

4. Hypovolaemia – vomitting + osmotic diuresis

Increases concentration of ketones + glucose

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

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

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*

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.

Christian.Hariman@uhcw.nhs.uk

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

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