This document provides an overview of endocrine emergencies, including diabetic emergencies like diabetic ketoacidosis and hypoglycemia. It also covers other metabolic disorders such as thyrotoxicosis, Addisonian crisis, and electrolyte abnormalities. For each condition, it describes the symptoms, pathophysiology, diagnosis, and treatment approach. The goal is to help recognize and initiate management of these urgent endocrine conditions.

1. Endocrine
Emergencies
Dr WAEL A. ELADL

2. 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

3. Diabetes Emergencies
 Diabetes Ketoacidosis
 Hyperosmolar Non Ketosis (Hyperosmolar
Hyperglycaemic state)
 Hypoglycaemia

4. Case
Rose Smith

5. Diabetic Ketoacidosis
(DKA)

6. Loss of Beta cell function in pancreas
beta-cell
alpha-cell
Loss of beta cell
function is gradual
over time
“Honeymoon period”

7. 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)

8. Diabetic
Ketoacidosis:Pathophysiology
Normal – glucose in
blood

9. Diabetic
Ketoacidosis:Pathophysiology
Normal Mechanism

10. 1. Insulin deficiency
*lack of glucose in muscle
2. glucagon excess
*increase in gluconeogenesis
Diabetic
Ketoacidosis:Pathophysiology

11. Diabetic
Ketoacidosis:Pathophysiology
3. Rapid lipolysis into free fatty acids
and ketone bodies
release of Beta-hydroxybutyrate
ketones makes you sick

12. Diabetic
Ketoacidosis:Pathophysiology
4. Hypovolaemia – vomitting + osmotic
diuresis
Increases concentration of ketones
+ glucose

13. 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)

14. 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

15. 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

16. 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

17. 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

18. 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

19. Case
Nicholas Brown

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

21. 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

22. HHS: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

23. Diagnosis
 Diagnosis requires ALL of the following:
 Raised blood glucose (usually >30mmol)
 Absence of ketones (or + or ++ only)
 Serum osmolality >350mmol

24. 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

25. 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

26. Case
Daniel Walters

27. Hypoglycaemia

28. Causes
 Insulin / medications
 Liver disease
 Insulinoma

29. 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*

30. 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

31. 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

32. Case
Joanna Webbley

33. Thyrotoxicosis

34. 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 )

35. Causes
 Graves Disease
 Thyroiditis (Hashimoto’s, de Quervain’s, etc)
 Primary hyperthyroid (multinodular goitre,
single nodule, etc)
 Exogenous thyroid

36. Diagnosis
 Free T4, Free T3 elevated
 TSH suppressed
 Thyroid antibodies (if autoimmune) present

37. 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

38. 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

39. Case
Brian Walker

40. Addison’s Disease
& Crisis

41. Hypothalamus-pituitary-adrenal axis
Hypothalamus
Pituitary
Adrenals
CRH
ACTH
GlucocorticoidsNegative feedback

42. 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

43. 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

44. 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

45. 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)

46. 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

47. Hyper + Hypo natraemia
 Assess patient’s fluid status
 Hypovolaemia, euvolaemia, hypervolaemia
 Hypernatraemia
 Hyponatraemia
 Beware of acute vs chronic
hyper/hyponatraemia

48. 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

49. Hypernatraemia
 Assess fluid status
 Commonest cause is pure water loss
 Chronic vs acute
 Investigate cause: Conn’s, Diabetes insipidus
 Fluid replacement – slowly if chronic

50. 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)

51. 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

52. Thank you
Christian.Hariman@uhcw.nhs.uk