Presented by:Session

ANP RAM Dr. Stacy

27 AprilArvinna
2023

Department Dr :Ryan
Emergency,
Cracknell HDOK.
 Pituitary apoplexy

1. Thyroid storm
Parathyroid gland Hypo / hypercalcaemia
2. Myxoedema coma

1. Addisonian Crisis
2. Phaeochromocytoma 1. Hypoglycaemia
hypertensive crisis 2. Diabetic Ketoacidosis
3. Hyperosmolar
Hyperglycaemic State
OVERVIEW
DIABETIC KETOACIDOSIS
HHS
HYPOGLYCEMIA
THYROID STORM
MYXEDEMA COMA
ADRENAL INSUFFICIENCY
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 : Physical findings:
- Polyuria - Dehydration
- Polydipsia - Hypotension
- Weight loss - Tachycardia
- Vomiting - Poor skin turgor
- Abdominal pain - Precipitating causes
- Weakness present (infection,
- Tachypnea vascular events, drug
- Altered mental status 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
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 mmol (2 ampules) of
bicarbonate in 200 ml of water with 20 meq of potassium chloride over two hours.
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 (HHS) is caused
by deficiency of insulin usually in elderly patients; 2/3
have previously undiagnosed diabetes
Mortality up to 50%
Diagnostic criteria:
Hypovolaemia
hyperglycaemia (BG>30mmol/L)
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
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

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
chlorpromazine
2. Tumours
- Insulinoma
- Retroperitoneal sarcomas

3. Miscellaneous
- Liver dysfunction
- adrenal insufficiency / hypopituitarism
- renal failure
- myxoedema
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 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 neuro-psychiatric
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.
Uncomplicated Thyrotoxicosis
Heat intolerence, diaphoresis
Sinus tachycardia, Heart rate 100-140
Diarrhea, increase appetite with loss
of weight
Anxiety, restlessness
Thyroid Storm
Hyperpyrexia, temperature >38.5C,
dehydration
HR >140bpm, hypotension, atrial
dysrhythmias, congestive heart
failure
Nausea, vomitting, severe diarrhea,
abdominal pain, hepatocellular
dysfunction-jaundice
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 Peripheral

release of thyroid conversion
hormone (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
sympathetic outflow, decrease production of thyroid
hormone, and decrease peripheral conversion of T4 to T3.
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 thyroid-stimulating 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, ascites
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 L-thyroxine
300-400 ug given orally via nasogastric tube or
parenterally if available. Alternatively, doses of tri-
iodothyronine 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 5-10%
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 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