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ENDOCRINE
EMERGENCIES
A. Tuthill
February 2011
INTRODUCTION (1)

Endocrine emergencies comprise approx. 1.5% of
all hospital admissions in the UK

Diabetes mellitus is by far the most common
endocrine disorder encountered in clinical practice
- Type 2 diabetes affects 5% population
- Type 1 diabetes affects 0.5 – 1% population
INTRODUCTION (2)

The most common endocrine emergencies therefore
relate to diabetes and are
1. Hypoglycaemia
2. Diabetic Ketoacidosis
3. Hyperosmolar Hyperglycaemic State
INTRODUCTION (3)

The other emergencies which are life-threatening
and frequently overlooked
- Acute adrenal insufficiency
- Pituitary apoplexy
- Phaeochromocytoma hypertensive crisis
- Thyroid storm
- Myxoedema coma
- Hypo / hypercalcaemia
HYPOGLYCAEMIA



In 2004-5 there were approx. 8,000 hospital
admissions related to hypoglycaemia
However there can be up to 90,000 ambulance
callouts per year for this condition
ALL UNCONSCIOUS PATIENTS SHOULD BE
ASSUMED TO BE HYPOGLYCAEMIC UNTIL
PROVEN OTHERWISE
HYPOGLYCAEMIA (1)
Causes :
1. Drugs
- insulin/oral hypoglycaemics
- alcohol
- salicylates
- quinine
- beta-blockers, pentamidine, disopyramide
- prescription errors e.g. chlorpropamide for
chlorpromazine

HYPOGLYCAEMIA (2)
Causes :
2. Tumours
- Insulinoma
- Retroperitoneal sarcomas

3. Miscellaneous
- Liver dysfunction
- adrenal insufficiency / hypopituitarism
- renal failure
- myxoedema
HYPOGLYCAEMIA (3)
Presentation :
1. Autonomic (Blood glucose 3.3 – 3.6 mmol/l)
- diaphoresis
- anxiety
- palpitations / tachycardia
- tremor
- warm feeling

HYPOGLYCAEMIA (4)
Presentation :
2. Neuroglycopenic (Blood glucose <2.6 mmol/l)
- confusion
- slurred speech
- visual disturbances
- being uncoordinated
- tiredness
- focal neurological defects
- coma / seizures (usually with glucose <1.5
mmol/l)

HYPOGLYCAEMIA (5)

Hypoglycaemia unawareness occurs in up to 1/3
patients with type 1 diabetes

Conversely, some patients have hypoglycaemic
symptoms when their glucose is above the target
range (> 7.0 mmol/l)

Patients post total pancreatectomy have more
frequent and severe episodes because they have
also lost their glucagon producing cells
HYPOGLYCAEMIA (6)

Diagnosis :
- Blood glucose
- U and E, liver profile
- Insulin and C-peptide levels
- Sulphonylurea screen
- IGF-2
HYPOGLYCAEMIA (7)

Treatment :
- If the patient is conscious, treat orally
- If unconscious, give 50ml 50% dextrose IV
- Glucagon 1mg i.m.
- Infusion of 10% glucose
- Consider thiamine
- Vigilance, Re-education, Support
HIGHS
LOWS
DIABETIC KETOACIDOSIS


DKA is a triad of hyperglycaemia, ketosis and
acidaemia
Diagnostic criteria (ADA) :
- Blood glucose > 13.8 mmol/l
- pH < 7.3
- Serum bicarbonate < 18mmol/l,
- Anion gap > 10
- Ketonaemia
DIABETIC KETOACIDOSIS (1)

EURODIAB study reported an incidence of DKA in
type 1 diabetes of 8.6%

It is the most common cause of death in young
people with diabetes and in those > 65 years of age

Precipitants include infection, MI, trauma, drugs
(steroids, cocaine, antipsychotics), non-compliance.
It may also be the presenting feature of type 1
diabetes

DIABETIC KETOACIDOSIS (2)

Pathogenesis :
- insulin deficiency
- increased counter-regulatory hormones (glucagon,
catecholamines, cortisol and GH)

This leads to increased glucose production by the
liver and decreased utilisation in peripheral tissues.
Lipolysis results in ketone body production and
acidosis.
DIABETIC KETOACIDOSIS (3)

Clinical Features :
- Polyuria
- Polydipsia
- Weight loss
- Vomiting / abdominal pain
- Dehydration
- Tachypnoea
- Altered mental status
DIABETIC KETOACIDOSIS (4)

Laboratory Findings :
- Hyperglycaemia (> 13.8 mmol/l)
- Hyperosmolality [2x(Na+K) + Urea + Glucose]
- Ketones
- Widened anion gap metabolic acidosis (pH < 7.3)
- Elevated urea and creatinine
- Hyperkalaemia
- Leucocytosis
DIABETIC KETOACIDOSIS (5)

Management :
- FLUIDS
- Fluids
- Fluids
- INSULIN
- POTASSIUM
- ± ICU admission
- Search for precipitant
- Education
HYPEROSMOLAR HYPERGLYCAEMIC STATE



Hyperosmolar hyperglycaemic state (HHS) is
caused by deficiency of insulin usually in elderly
patients; 2/3 have previously undiagnosed diabetes
Mortality up to 50%
Diagnostic criteria:
- Blood glucose > 33.3 mmol/l
- pH > 7.3
- Serum bicarbonate > 15 mmol/l,
- Serum Osmolality > 320mOsm/Kg
HYPEROSMOLAR HYPERGLYCAEMIC STATE

Precipitants :
- Infection
- Myocardial infarction / cerebrovascular accident
- Inadequate insulin treatment / noncompliance
- High sugar intake
- Other endocrine disorders e.g. acromegaly
- Drugs e.g. glucocorticoids, thiazides, loop
diuretics, phenytoin
HHS (2)

Clinical Features :
- Similar to DKA but history often several days to
weeks
- As the degree of hyperglycaemia and
hyperosmolarity progresses neurologic
symptoms are more common including lethargy,
focal signs, obtundation and coma
- Severe dehydration
HHS (3)

Laboratory Findings :
- Hyperglycaemia
- Hyperosmolarity [2x(Na+K) + Urea + Glucose]
- Hypo or hypernatraemia
- Hyperkalaemia
HHS (4)

Management :
- FLUIDS
- Fluids
- INSULIN
- POTASSIUM
- Anticoagulation
- ± ICU admission
- Search for precipitant
- Education
ACUTE ADRENAL INSUFFICIENCY


Life-threatening emergency
Causes :
- Autoimmune
- Adrenal TB / haemorrhage / metastases
- Hypopituitarism
- Drugs e.g. metyrapone, ketoconazole, rifampicin
- Interruption of adrenal replacement therapy
- Adrenoleucodystrophy
ACUTE ADRENAL INSUFFICIENCY(1)

Clinical Features :
- Hypotension (mineralocorticoid deficiency)
- Postural hypotension
- Nausea and vomiting, weight loss, fatigue
- Hypoglycaemia
- Hyperpigmentation
ACUTE ADRENAL INSUFFICIENCY(2)

Laboratory Findings:
- Hyponatraemia (90%) / hyperkalaemia (65%)
- Elevated Urea
- Hypoglycaemia
- Anaemia (normal MCV)
- Metabolic acidosis
- Hypocortisolaemia / Failure to respond adequately
to synthetic ACTH
- ACTH or 
-  Plasma renin
ACUTE ADRENAL INSUFFICIENCY(3)

Management :
- Intravenous fluids (Saline)
- Steroids
- Dextrose
- Evaluate cause (antibodies, imaging, VLCFA)
- Investigate for other endocrinopathies
- Steroid alert card / bracelet
- Education
PHAEOCHROMOCYTOMA /
CATECHOLAMINE CRISIS






Phaeochromocytomas are catecholamine secreting
tumours of the adrenal medulla
< 0.1% Hypertension, but may cause hypertensive
emergencies (SBP > 220mmHg or DBP > 120 mmHg)
10% bilateral
10% extra-adrenal
10% malignant
10% familial (Neurofibromatosis, Von Hippel Lindau,
MEN 2, SDHD/SDHB mutations)
PHAEOCHROMOCYTOMA /
CATECHOLAMINE CRISIS(1)

Secretory Products:
- Noradrenaline / normetanephrines
- Adrenaline / metanephrines
- Dopamine
PHAEOCHROMOCYTOMA /
CATECHOLAMINE CRISIS(2)

Clinical Features :
- Hypertension
- Anxiety attacks
- Sweating and heat intolerance
- Flushing / Pallor, palpitations, pounding
headaches, pyrexia
- Tachycardia / arrhythmias
PHAEOCHROMOCYTOMA /
CATECHOLAMINE CRISIS(3)

Crisis Precipitants :
- Straining
- Exercise
- Pressure on abdomen
- Surgery
- Drugs
PHAEOCHROMOCYTOMA /
CATECHOLAMINE CRISIS(4)

Laboratory Findings :
- Hyperglycaemia
- Hypokalaemia

Investigations :
- Urinary catecholamines
- Chromogranin A, B
- MRI / MIBG
PHAEOCHROMOCYTOMA /
CATECHOLAMINE CRISIS(5)

Management :
- Rehydration
- Alpha blockade (Phentolamine /
phenoxybenzamine)
- LATER, Beta blockade
- Surgical resection
- Screening for associated conditions
PITUITARY APOPLEXY

Apoplexy refers to infarction of the pituitary gland
due either to haemorrhage or ischaemia

Causes :
- Spontaneous haemorrhage
- Anticoagulant therapy
- Head trauma
- Radiation therapy
- Drugs (Bromocriptine)
- Pituitary function testing
PITUITARY APOPLEXY(1)



Rare
0.6 – 25% cases of treated pituitary adenoma
Clinical Features :
- Headaches
- Nausea, vomiting
- Visual disturbance
- Cranial nerve palsy
- Meningism
PITUITARY APOPLEXY(2)

Diagnosis :
- High degree of suspicion
- Brain imaging
- Hypo / hypernatraemia may occur
- Baseline pituitary function tests
- Visual fields
PITUITARY APOPLEXY(3)

Management :
- Stabilise the patients (A, B, C)
- Hydrocortisone
- Fluid balance
- Early neurosurgical intervention particularly if
significant visual involvement
- Reassess pituitary function once acute apoplexy
resolved
HYPOCALCAEMIA

Usually the result of failure of PTH secretion or
inability to release calcium from bone

Causes :
- Hypoparathyroidism (autoimmune, surgical,
radiation, infiltration)
- Failure of parathyroid development
- Failure of PTH secretion (Magnesium deficiency)
- Failure of parathyroid action
(Pseudohypoparathyroidism)
HYPOCALCAEMIA(1)

Causes : (contd.)
- Failure of 1,25 (OH)2D levels (drugs, pancreatitis)
- Failure of calcium release from bone
(osteomalacia, renal failure, hungry bone syndrome)
- Complexing of calcium from the circulation
(multiple blood transfusion, pancreatitis)
HYPOCALCAEMIA(2)

Clinical Features :
- Tingling and numbness espec. of fingers, toes or
lips
- Cramps
- Carpopedal spasm
- Tetanic contractions (may include laryngospasm)
- Seizures
- Hypotension, bradycardia, arrhythmias, CCF
Trousseau’s Sign
HYPOCALCAEMIA(3)

Investigations :
- Plasma calcium, albumin and phosphate
- Magnesium
- U and E’s
- PTH
- ECG
- 25 (OH) Vit D
HYPOCALCAEMIA(4)

Management :
- Patients with tetany or seizures require urgent
intravenous treatment with calcium gluconate
followed by an infusion for maintenance
- Chronic hypocalcaemia is best managed with oral
calcium and vitamin D
HYPERCALCAEMIA

Found in 5% hospital patients but only 0.5% general
population

Frequently picked up by routine biochemical screen
in an asymptomatic patient
HYPERCALCAEMIA(1)

Causes :
- Hyperparathyroidism
- Malignancy
- Hyperthyroidism
- Sarcoidosis
- Drug related (thiazides, vitamin D, lithium)
- Immobilisation
- Miscellaneous (Benign Familial Hypocalciuric
Hypercalcaemia)
HYPERCALCAEMIA(2)

Clinical Features :
- Polyuria, polydipsia, dehydration
- Tiredness, weakness, anorexia, malaise, nausea
- Abdominal pain, constipation
- Confusion, lethargy, depression
- Renal calculi, renal failure
- Sudden cardiac arrest
HYPERCALCAEMIA(3)

Investigations :
- Plasma Calcium (corrected for albumin)
- Phosphate, Magnesium
- U and E’s
- LFT’s
- PTH
- 24 hr urine Calcium
- ECG
HYPERCALCAEMIA(4)

Additional Investigations :
- Myeloma screen
- TFT’s
- Short synacthen test
- Renal US
- DEXA
HYPERCALCAEMIA(5)

Management :
- Rehydration (Saline)
- ± Loop diuretic
- IV Bisphosphonate
- Salmon calcitonin
- Steroids
SUMMARY

Most endocrine emergencies encountered by
general physicians relate to hyperglycaemia and
hypoglycaemia in diabetes

The remaining endocrine emergencies are very rare

Treatment should never be delayed for a
confirmatory test

CONSIDER THE DIAGNOSIS