Endocrine

Emergencies
Christian Hariman

Objectives

Diabetic Emergencies
Recognise and participate in the management of diabetic
ketoacidosis
Recognise and participate in the initial management of honk
Recognise and manage hypoglycaemia

Other Metabolic Disorders

Recognise the symptoms and signs of thyrotoxicosis
Manage thyrotoxicosis using medical therapy
Recognise and initiate the immediate management of
Addisonian crisis
Initiate investigation of hypo and hyper natraemia and hypo
and hyperkalaemia initiate management of these conditions
Recognise the circumstances when hypercalcaemia may
occur and initiate the management of hypercalcaemia

Diabetes Emergencies

Diabetes Ketoacidosis
Hyperosmolar Non Ketosis
(Hyperosmolar Hyperglycaemic
state)
Hypoglycaemia

Case
Rose Smith

Diabetic
Ketoacidosis
(DKA)

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:Pathophysio
logy

M
US
C

LE

Normal glucose in
blood
O

Ketoacidosis:Pathophysio
logy

M
US
C

LE

Normal Mechanism
L

In
su
lin

Ketoacidosis:Pathophysio
logy
er
Liv

Glucagon

1.
B

M
US
C

*lack of glucose in muscle

O

2.
LE

Insulin deficiency

glucagon excess
*increase in gluconeogenesis

In
su
lin

Ketoacidosis:Pathophysio
logy
3. Rapid lipolysis into free fatty acids
and ketone bodies
B
keto

release of Beta-hydroxybutyrate

nes

M
US
C

ketones makes you sick

LE
keto

nes

Ketoacidosis:Pathophysio
logy
keto

nes

M
US
C

4. Hypovolaemia vomitting + osmotic

diuresis
B

D
keto
nes

LE

Increases concentration of ketones

+ glucose

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.
2.
3.
4.
5.
6.
7.

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
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
Insulin
infusion
50units actrapid
made to 50ml with NaCl
0.9%

Rate: 0.1 units/kg/hour

E.g 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

Serum K+ 3.5 - 5.4

Add 20mmol per litre

Serum K+ <3.5

No potassium supplement

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

Case
Nicholas Brown

Hyperosmolar
Hyperglycaemic
State (HHS)
(the artist formerly known as
Hyperosmolar Non Ketotic
HONK)

Features of HHS

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 higher than DKA

HHS:Pathophysiology
1.
B

M
US
C

LE

No switch to fat metabolism

and therefore no ketones or
acidosis

In
su
lin

Insulin production markedly

reduced but NOT absent.

2.

Gluconeogenesis

3.

Loss of intravascular volume

Diagnosis

Diagnosis requires ALL of the

following:

Raised blood glucose (usually >30mmol)

Absence of ketones (or + or ++ only)

Serum osmolality >350mmol

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

More insulin sensitive

Reduce rate if Blood glucose falls >10
mmol / hour

70kg = 7 units/hour

Consider halving the rate within the first 1-2

hours

Stop when patient is recovered

Case
Daniel Walters

Hypoglycaemia

Causes

Insulin / medications
Liver disease
Insulinoma

Features of
Hypoglycaemia

Autonomic:
sweating, palpitations, tremor, hunger
Neuroglycopenic
confusion, clumsiness, behavioural changes,
seizures
Non-specific
nausea, headache, tiredness
Symptoms may not present at the same level of
blood glucose
Diagnosis with serum/capillary glucose (<3.0)

*beware may not be accurate*

Treatment of
hypoglycaemia

If able to eat
glucose: e.g 3 dextrosol tabs / 200mls of
orange juice/ sugar drinks
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

Other Metabolic
Disorders

Thyrotoxicosis
Addisonian Crisis

Initiate investigation of hypo and hyper

natraemia and hypo and hyperkalaemia initiate
management of these conditions

Recognise the circumstances when

hypercalcaemia may occur and initiate the
management of hypercalcaemia

Case
Joanna Webbley

Thyrotoxicosis

Thyrotoxicosis

Sweating
Tachycardia with or without AF
Nausea, vomiting and diarrhea
Tremulousness and delirium,
occasionally apathetic
Diarrhoea
Exopthalmos (only in graves disease)
Hyperpyrexia ( >40 0C )

Causes

Graves Disease
Thyroiditis (Hashimotos, de
Quervains, etc)
Primary hyperthyroid (multinodular
goitre, single nodule, etc)
Exogenous thyroid

Diagnosis

Free T4, Free T3 elevated

TSH suppressed
Thyroid antibodies (if autoimmune)
present

Treatment

Anti-thyroid medication
Carbimazole (CMZ), Propylthiouracil
(PTU)
Beware of CMZ in pregnancy
Beware of aggranulocytosis

Beta blocker
CMZ / PTU takes 2 weeks
Beta blockade patient if symptomatic for
2-3 weeks

Thyroid Storm

rare
A-E of resuscitation, treat
hyperthermia
Call senior help / ITU
May require parentral beta blockade
and anti-thyroid medications
Can give lugol iodine to block
thyroid release

Case
Brian Walker

Addisons
Disease
& Crisis

Hypothalamus-pituitaryadrenal axis
Hypothalam
us
CRH
Pituitary

ACTH

Adrenals
Negative
feedback

Glucocorticoid
s

Features

rare
Lack of cortisol
Orthostatic hypotension, lethargy, faintings
If autoimmune dark/pigmented skin
Causes:

Iatrogenic : Adrenelectomy, sudden stop of long

term glucocorticoids
Autoimmune
Hypothalamic disease, pituitary disease, adrenal
disease

Diagnosis

Low random cortisol (not accurate)

Short Synachten test
Cortisol time 0
Synacthen (artificial ACTH)
Intramuscular
Cortisol time 30 mins

Interpretation

Normal: increment of >200 nmol/L and

30min test >600 nmol/L

Treatment

Give Cortisol
Intravenous 200 mg Hydrocotisone
Oral Hydrocortisone
10mg 10/5mg 5mg routine
Normal adult required 20-30mg HC daily

Remember:
Sick patients require more cortisol
5mg Prednisolone = 20mg Hydrocortisone
STEROID CARD

Hyperkalaemia

Normal range 3.5 4.5

Danger of atrial / ventricular
fibrillation
Assess patient (A-E of resus)
Re-check the Potassium levels (lab +
blood gas)
Stop offending drugs
(spironolactone, amiloride)

Hyperkalaemia
treatment

Urgent

ECG tall t waves / widening QRS

Cardiac compromise or impending

Emergency call if cardiac compromise

10mL Calcium gluconate (10%) over 2 min

50mL of 50% dextrose + 10 units Actrapid over 20-30
mins
Consider dialysis / filtration

Non urgent

Nebulised Salbutamol
Calcium resonium
50mL of 50% dextrose + 10 units Actrapid over 20-30
mins

Hyper + Hypo natraemia

Assess patients fluid status

Hypovolaemia, euvolaemia,
hypervolaemia
Hypernatraemia
Hyponatraemia

Beware of acute vs chronic

hyper/hyponatraemia

Hyponatraemia

Common in elderly
If asymptomatic + chronic may not need treatment
Investigate cause: Addisons, SIADH
Consider stopping the offending drug
ACE-i, diuretics, omeprazole
Main treatment:

Fluid restrict if euvolaemia / hypervolaemia

If unable to tolerate consider V2 receptor antagonist
If hypovolaemia slow fluid resuscitation
BEWARE too quick replacement can cause Central
Pontine Myelinolysis

Hypernatraemia

Assess fluid status

Commonest cause is pure water loss
Chronic vs acute
Investigate cause: Conns, Diabetes
insipidus
Fluid replacement slowly if chronic

Hypercalcaemia

Behavioural change, tetany, seizures

Investigate cause Primary
hyperPTH, malignancy, recent bone
radiotherapy, Familial Hypercalcaemia
hypocalciuria
Beware of true calcium levels in
hypoalbuminaemia

Corrected Ca = measured Ca + 0.02 x

(40-albumin)

Hypercalcaemia

Treat underlying cause if possible

ABC of resus
IV fluids
Correct hypomagnasaemia /
hypokalaemia
Consider diuretics once rehydrated
Bisphosphonates takes 2-3 days, max 1
week

Inhibits osteoclast + bone resorption

Thank you
Christian.Hariman@uhcw.nhs
.uk