Diabetes

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

 Todays 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 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

Loss of beta cell

function is gradual
over time
Honeymoon period
alpha-cell

beta-cell
 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)
Ketoacidosis:Pathophysiolo
gy

Normal glucose in
B blood
L
O
O
D

M
US
CL
E
Ketoacidosis:Pathophysiolo
gy

Normal Mechanism
B
L
O
O
D

M
US
CL
E
In
su
lin
Ketoacidosis:Pathophysiolo
gy
Glucagon
er
Liv

1. Insulin deficiency
B
L *lack of glucose in muscle
O
O
D
2. glucagon excess
M
US
CL *increase in gluconeogenesis
E
In
su
lin
Ketoacidosis:Pathophysiolo
gy

3. Rapid lipolysis into free fatty acids

and ketone bodies
B
L
O
O release of Beta-hydroxybutyrate
D
keto
nes
M
US ketones makes you sick
CL
E
keto
nes
Ketoacidosis:Pathophysiolo
gy

4. Hypovolaemia vomitting + osmotic

keto
nes
diuresis
B
L
O
O Increases concentration of ketones
D
+ glucose
M keto
US nes
CL
E
 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 / insulin
4. Replace electrolytes
5. Look for cause
6. Close monitoring
7. Consider Low molecular weight heparin
Replacing fluids
Initial management Later

1L 0.9% NaCl Once blood glucose <14

30 mins* mmol/L give 10%
1hr dextrose alongside 0.9%
2hr Normal Saline at 125ml /
4 hr hour

Then continue NaCl 0.9%

as dictated by fluid status

*beware of elderly patients

Resolution of ketonaemia
Insulin 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 doesnt mean absence of infection

Consider alternative cause for acidosis if glucose and acidosis

markedly out of proportion

Non specific abdo pain and raised amylase doesnt always mean
pancreatitis

Do not stop insulin even if the blood glucose is normal or below

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-
Ketotic
Hyperglycaemic State
(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
HONK:Pathophysiology

1. Insulin production markedly

reduced but NOT absent.

B No switch to fat metabolism

L
O and therefore no ketones or
O
D acidosis

M 2. Gluconeogenesis
US
CL
E 3. Loss of intravascular volume
In
su
lin
 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?

Fluid replacement SLOWER (may be a 1L 0.9% NaCl

marker of population not pathology) 1 hr*
Electrolyte replacement 2 hr
(pseudohyponatraemia) 4 hr
8 hr
Insulin slower scale normally very
responsive to IV insulin
Then continue NaCl 0.9% as
Search for cause dictated by fluid status
ANTICOAGULATION
Monitor
*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

Hypoglycaemia
 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