ENDOCRINE

EMERGENCIES
Presented by: Dr. Stacy Arvinna
Department : Emergency, HDOK.

Pituitary apoplexy

1. Thyroid storm
2. Myxoedema coma

1. Addisonian Crisis
2. Phaeochromocyto
ma hypertensive
crisis

Parathyroid gland
Hypo / hypercalcaemia

1.
2.
3.

Hypoglycaemia
Diabetic Ketoacidosis
Hyperosmolar
Hyperglycaemic State

OVERVIEW
DIABETIC KETOACIDOSIS
HHS
HYPOGLYCEMIA
THYROID STORM
MYXEDEMA COMA
ADRENAL INSUFFICIENCY

DIABETIC
KETOACIDOSIS

DIABETIC KETOACIDOSIS
DKA is a triad of hyperglycaemia, ketosis and

acidaemia
DKA is a potentially life threatening medical emergency
due to absolute or relative insulin deficiency coupled
with counter-regulatory hormones excess.
Diagnostic criteria (ADA) :
- Blood glucose > 13.8 mmol/l
- pH < 7.3
- Serum bicarbonate < 18mmol/l,
- Anion gap > 10
- Ketonaemia

Clinical Features :

- Polyuria
- Polydipsia
- Weight loss
- Vomiting
- Abdominal pain
- Weakness
- Tachypnea
- Altered mental
status

Physical findings:
Dehydration
Hypotension
Tachycardia
Poor skin turgor
Precipitating causes

present (infection,
vascular events,
drug abuse etc)

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

Differential diagnosis.
Hyperglycemic hyperosmolar state is not

associated with ketosis.

Starvation and alcoholic ketoacidosis are not
characterized by hyperglycemia >200 mg/dl and
bicarbonate level <18 meq/L.
With hypotension and history of metformin use,
lactic acidosis (lactic acid level >7 mmol/L)
should be suspected.
Ingestion of methanol, isopropyl alcohol, and
paraldehyde can also alter anion gap and/or
osmolality and need to be investigated.

Management
A.Fluid therapy
B.Insulin infusion
C.Electrolyte management
D.Treatment of underlying cause

According to ENDOCRINE UNIT HOSPITAL UNIVERSITI SAINS MALAYSIA KOTA BHARU,

KELANTAN

FLUID THERAPY
Fluid replacement is priority one in the treatment of DKA.
Replace fluid deficit in DKA (~6 L) within 24-36 hours with the goal
of 50% volume replacement within first 12 hours.
Rate

Action

Fluid

Step 1

1 pint over 30
min for 1 hour

To review

1 litre

Step 2

1 pint over 1
hour for 2 hour

To review

1 litre

Step 3

1 pint over 2
hour for 4 hour

To review

1 litre

Step 4

1 pint over 4
hour for 8 hour

To review

1 litre

INSULIN INFUSION
Start IVI at 0.1 unit/kg/ hr based on estimated body weight
(50 units human soluble insulin;Actrapid/ Humulin R + 0.9%
NaCl= 50 ml)
Irrespective of blood glucose level
Bolus insulin is not recommended
Monitor blood glucose level hourly
Aim for blood glucose drop of 2-4mmol/L per hour
Initially, aim for CBG~10mmol/L (range 8-12mmol/L)

until DKA has improved

oWithold insulin infusion if serum potassium <3.5mmol/L or ECG changes of
hypokalaemia.
o Transition to SC insulin by giving long-acting insulin 2 hours before the
discontinuation of IV insulin.

ELECTROLYTE MANAGEMENT
Potassium
Begin preplacement at the second hour of fluid therapy
Start with 0.5 gm KCL per hour over 2 hour (eg. Add 0.5gm KCL in
1 pint of normal saline and run over 1 hour for 2 hour).
Once result is available, replace according to the result
Aim-Serum Potassium 4.0-5.0mmol/L
Sodium
If serum sodium is normal, use 0.9% NaCl(normal saline) in fluid
therapy
If elevated (>160mmol/L) use 0.45% NaCl (half normal saline) in
fluid therapy
Bicarbonate
Bicarbonate replacement is not routinely indicated in the
management of DKA
Consider giving bicarbonate replacement if pH <7.0 and/or serum
bicarbonate <10mmol/L
if pH is < 7.0 or bicarbonate level is < 5 meq/L, administer 100

Outline monitoring
regimen
Hourly capillary blood glucose
Vital signs and input-output charting hourly
Venous bicarbonate and potassium at

60minutes, 4 hours and 6-hourly thereafter

6-hourly plasma electrolytes and urine ketone
Continuous pulse oximetry (if indicated)
Continuous cardiac monitoring (if indicated)
Look for precipitating cause and start broad
spectrum antibiotic if infection suspected.

HYPEROSMOLAR
HYPERGLYCAEMIC
STATE

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:

Hypovolaemia
Marked hyperglycaemia (BG>30mmol/L)
Osmolality >320 mosmol/kg

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

Laboratory Findings :

- Hyperglycaemia
- Hyperosmolarity [2x(Na+K) + Urea +
Glucose]
- Hypo or hypernatraemia
- Hyperkalaemia

HYPOGLYCEMIA

HYPOGLYCAEMIA
IN CONTEXT OF DIABETES; excess insulin in absence

of enough carbohydrate. Most common in insulin

treated patient.
Low blood glucose concentrations lead to adrenergic
activation and neuroglycopenia .
Symptomatic hypoglycemia is diagnosed clinically
using Whipples triad: symptoms of hypoglycemia,
plasma glucose concentration<50 mg/dl (2.8 mmol/l),
and resolution of those symptoms after the plasma
glucose concentration is raised.
ALL UNCONSCIOUS PATIENTS SHOULD BE ASSUMED
TO BE HYPOGLYCAEMIC UNTIL PROVEN OTHERWISE

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

PATHOPHYSIOLOGY
Redundant counter-regulatory mechanisms are in
place to prevent or correct hypoglycemia. As glucose
levels decline, major defenses include:
1) a decrease in insulin secretion;
2) an increase in glucagon secretion;
3) an increase in epinephrine secretion. Increased
cortisol and growth hormone secretion also occur.
If these defenses fail, plasma glucose levels will
continue to fall.
In type 1 and longstanding type 2 diabetes these counter-regulatory
responses to hypoglycemia are frequently impaired. This increases the
risk of hypoglycemia and also contributes to hypoglycemia unawareness.

Causes :
1. Drugs
- insulin/oral hypoglycaemics
- alcohol
- salicylates
- quinine
- beta-blockers, pentamidine, disopyramide
- prescription errors e.g. chlorpropamide for
2. Tumours
- Insulinoma
- Retroperitoneal sarcomas
3. Miscellaneous
- Liver dysfunction
- adrenal insufficiency / hypopituitarism
- renal failure
- myxoedema

chlorpromazine

Presentation :
1. Autonomic (Blood glucose 3.3 3.6 mmol/l)
- diaphoresis
- anxiety
- palpitations / tachycardia
- tremor
- warm feeling
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)

Diagnosis :

Blood glucose
U and E, liver profile
Insulin and C-peptide levels
Sulphonylurea screen
IGF-2

THYROID STORM

Thyroid gland

Thyroid Storm
A life threatening exacerbation of the

hyperthyroid state with evidence of

decompensation in one or more organ
systems. The mortality is 20 - 30 %.
It may be precipitated by stress including
concurrent infections, surgery or pregnancy.
It is a clinical diagnosis with features of
severe thyrotoxicosis, hyperpyrexia and neuropsychiatric manifestations such as delirium.
Malaysian Endocrine and Metabolic Society (MEMS)

Precipitating factors
General:
Infection.
Non-thyroidal trauma or surgery.
Psychosis.
Parturition
DKA

Myocardial infarction or other acute medical problems.

Thyroid specific:
Radioiodine.
High doses of iodine-containing compounds (for example,
radiographic contrast media).
Discontinuation of antithyroid drug treatment.
Thyroid injury (palpation, infarction of an adenoma).
New institution of amiodarone therapy.

Scoring.
<25 : unlikely thyroid
storm
25-44 : supports the
diagnosis
>45 : highly suggestive
of thyroid storm
Adapted from: Burch HB, Wartofsky L. Life
threatening thyrotoxicosis. Thyroid storm.
Endocrinol Metab Clin North Am 1993:
22:263

Laboratory investigation
Free T4, free T3 elevated
TSH suppressed
Note that findings are not different than that

of hyperthyroidism, but the difference is in the

setting
Biochemical features
include hyperglycaemia, leucocytosis, mild
hypercalcaemia,
and abnormal liver function tests.

How to differentiate ??
Uncomplicated
Thyrotoxicosis

Thyroid Storm

Heat intolerence, diaphoresis

Hyperpyrexia, temperature
>38.5C, dehydration

Sinus tachycardia, Heart rate

100-140

HR >140bpm, hypotension,
atrial dysrhythmias, congestive
heart failure

Diarrhea, increase appetite

with loss of weight

Nausea, vomitting, severe

diarrhea, abdominal pain,
hepatocellular dysfunctionjaundice

Anxiety, restlessness

Confusion, agitation, delirium,

frank psychosis, seizures,
stupor or coma

Management of Thyroid Storm

Asses ABCDE
Rehydration
Treat hyperpyrexia (use fans,

tepid sponging and oral

paracetamol)
Do NOT use aspirin or NSAIDs

Treatment of Thyroid
Storm
Sympathetic
outflow

Triangle
of
Treatment

Production and
release of thyroid
hormone

Peripheral
conversion
(T4 T3)

Management of Thyroid
Storm
Beta sympathetic blocking agents
o Oral propanolol 40 mg qid, or I/V 1-2 mg 4-6 hourly
Iodide
o Oral saturated solution of potassium iodide (SSKI)
5 drops 6-hourly
o or I/V Sodium Iodide 500 mg 8 hourly
o or oral Lugol's iodine 5-10 drops, 6-hourly
Antithyroid Drugs
o Carbimazole 15-20 mg 6-hourly
o or propylthiouracil 150-200 mg 6-hourly
Corticosteroids
o I/V dexamethasone 2 mg 6-hourly
o or I/V hydrocortisone 200 mg 6-hourly

Take home points

1.Patients susceptible to developing thyroid storm have
increased sensitivity to catecholamines. Therefore, any
stressor that leads to outpouring of catecholamines, can
lead to thyroid storm.
2.Thyroid storm is a true medical emergency; these
patients should be managed in the ICU and beta-blockers
should be started early (esmolol is a great choice
because of its short half-life (on the order of seconds).
3.Remember the triangle of treatment: decrease
sympathetic outflow, decrease production of thyroid
hormone, and decrease peripheral conversion of T4 to
T3.

MYXEDEMA COMA

Myxedema Coma
Severe hypothyroidism leading to decreased

mental status, hypothermia, and other symptoms

related to slowing of function in multiple organs.
It is a medical emergency with a high mortality
rate. Fortunately, it is now a rare presentation of
hypothyroidism, likely due to earlier diagnosis as
a result of the widespread availability of thyroidstimulating hormone (TSH) assays.
End stage of untreated or insufficiently treated
hypothyroidism
History:
Previous thyroid surgery
Radioiodine
Default thyroid hormone therapy

Precipitating factors
Hypothermia.
Infections especially pneumonia.
Myocardial infarction or congestive heart

failure.
Cerebrovascular accident.
Respiratory depression due to drugs (for
example, anaesthetics, sedatives,
tranquillisers).
Trauma or gastrointestinal blood loss

Pathogenesis of
Myxedema

Physical Findings
Comatose or semi

comatose
Dry coarse skin
Hoarse voice
Thin dry hair
Delayed reflex
relaxation time
Hypothermia
Pericardial,
pleural effusions,

Lab Tests
Free T4 low and TSH high
If the T4 is low and TSH low normal consider

pituitary hypothyroidism
Blood gasses
Electrolytes and creatinine
Distinguish from euthyroid sick syndrome
Low T3, Normal or low TSH, normal free T4

Management
1. ABCDE assesment
2. Gradual rewarming with blankets.
3. Accurate core temperatures should

be

recorded with a low reading Rectal

thermometer.
4. Thyroid hormone replacement with Lthyroxine 300-400 ug given orally via
nasogastric tube or parenterally if
available. Alternatively, doses of triiodothyronine 10 ug 8-hourly (IV or orally)
may be used.

5. I/V

hydrocortisone should be given, 200 mg

stat and 100 mg 6-hourly until patient regains
consciousness. Controversial but necessary in
hypopituitarism or multiple endocrine failure
6. Ensure adequate hydration and nutrition; Use 510% dextrose solution to maintain normal blood
glucose levels.
7. Correct electrolyte imbalance (patients tend to be
hyponatraemic).
8. Ensure adequate ventilation. Patients tend to
hypoventilate, resulting in hypercapnoea.
9. Treat precipitating cause.
10. Infection may be masked by the hypothyroid state.

ADRENAL GLANDS

Adrenal Gland

ACUTE ADRENAL INSUFFICIENCY

Clinical Features :

Hypotension (mineralocorticoid deficiency)

Postural hypotension
Nausea and vomiting, weight loss, fatigue
Hypoglycaemia
Hyperpigmentation

Clues to Underlying Chronic

Adrenal Insufficiency
Pigmentation in

unexposed areas
of the skin
Creases of hands
Buccal mucosa
Scars

Consider adrenal

insufficiency if
hypotension does
not respond to
pressors

Lab Tests
Hyponatremia and hyperkalemia

(Hyponatremia might be obscured by

dehydration)
Random cortisol is not helpful unless it is very
low (<5 mg/L) during a period of great stress

Lab Diagnosis

ACTH (cosyntropin) stimulation test

Failure of cortisol to rise above 552 nmol/L
30 min after administration of 0.25 mg of
synthetic ACTH IV
Basal ACTH will be raised in primary

adrenal insufficiency but not in secondary

CT of abdomen will reveal enlargement of
adrenals in patents with adrenal
hemorrhage, active TB or metastatic
malignancy

Management of Acute Adrenal

Insufficiency
ABCDE assesment
Hydrocortisone
100 mg IV stat then 50 mg 4 hly for 24 h
Taper slowly over the next 72 h
When oral feeds is tolerated change to oral
replacement therapy
Overlap the first oral and last IV doses
Replace salt and fluid losses with 5% dextrose

in normal saline IV

Patients with primary adrenal insufficiency

may require mineralocorticoid therapy

(fludrocortisone) when shifted to oral therapy
Treat precipitating diseases

SOURCES
Practice Guidelines For Thyroid Disorders The Malaysian

Consensus 2000
Postgraduate Medical Journal
Clinical Practice Guidelines Management Of Type 2 Diabetes
Mellitus(5th Edition) 2015
http://www.endotext.org
http://www.ncbi.nlm.nih.gov
www.medscape.org
Greenspan Fs. The Thyroid Gland Thyrotoxicosis Crisis. In Basic
And Clinical Endocrinology. Greenspan Fs, Gardner Dg, Eds. New
York: Lange Medical, 2001. Pp. 247-8
Hyperthyroidism: Management Guidelines Of The American
Thyroid Association And American Association Of Clinical
Endocrinology