‫‪Ministry of Higher Education And Scientific Research‬‬

‫‪Al-‬‬
‫‪Al-zahraa‬‬
‫‪zahraa Medical College‬‬

‫‪Endocrinology Emergencies‬‬
‫‪GROUP 3‬‬
‫عباس جميل عوده‬ ‫صبا محسن غالب‬ ‫ام البن‪ 6‬حس‪ 6‬علي‬
‫فاطمة كريم عبد‬ ‫عبدا‪ H‬ناهض حامد‬ ‫عبدا‪ H‬فراس شاكر‬
‫الرزاق‬
‫مصطفى احمد حسن‬ ‫محمد عبد الزهرة‬ ‫كوثر حميد محمد‬
‫رحمه‬
‫هبة سامي كاظم‬ ‫‪Medicine‬عبد‬
‫‪Internal‬‬ ‫موسى صالح‬
‫عباس‪12/9/2024‬‬ ‫مصطفى هيثم‬ ‫‪1‬‬

‫الرزاق‬
 LEARNING OBJECTIVES

1. Hypoglycemia
2. Diabetic Ketoacidosis (DKA)
3. Hyperosmolar Hyperglycemic State
4. Thyroid Storm
5. Myxedema Coma
6. Pheochromocytoma
7. Adrenal Crisis
8. Malignant hypercalcemia 2
A 34-year-old woman with known type 1 diabetes mellitus
was admitted to hospital following a ‘black out’ while
driving.
She had recently increased her insulin dose because she
felt unwell with ‘flu’ but unwisely had missed two meals
during the day. The results of some of her biochemistry
tests were as follows:
Loading…
Plasma Sodium 135 mmol/L (135–145)
Potassium 4.0 mmol/L (3.5–5.0)
Bicarbonate 23 mmol/L (24–32)
Urea 5.4 mmol/L (2.5–7.0) Creatinine 100 µmol/L (70–110) Glucose
1.5 mmol/L (5.5–11.1)
pH 7.43 (7.35–7.45)
PaCO 2 5.3 kPa (4.6–6.0)
PaO 2 12.1 kPa (9.3–13.3)
3
 Hypoglycemia
• In people with diabetes, hypoglycemia is defined as a
blood glucose of less than 3.9 mmol/L (70 mg/dL).
• When hypoglycemia develops in non-diabetic people, it
is called ‘spontaneous’ hypoglycemia.
Causes of Hypoglycemia
• Excess of insulin or oral hypoglycemic agents in a
known diabetic (most common)
• Drugs: insulin, insulin secretagogues
(chlorpropamide), alcohol, high doses of salicylates
• Critical illness
• Hormone deficiencies: adrenal insufficiency,
hypopituitarism
• Insulinoma (pancreatic β cell tumor), β cell hyperplasia 4
Clinical Features

Autonomic Autonomic Neuroglycopenic

(adrenergic)a (Cholinergic)
Palpitations Sweating Behavioral changes
Tremor Loading…
Hunger Speech difficulty
Anxiety Paresthesia Confusion
Drowsiness, Loss of
consciousness
Irritability, anger

5
 Investigation Normal
Also
3 .

9 mmoil L
• RBS : less than 70 mg/dl. If the glucose level is low and the
cause of hypoglycemia is unknown: include insulin,
proinsulin, C-peptide, sulfonylurea levels, cortisol, and
ethanol.
Severity of hypoglycemia
• Level 1 (alert value): (<70 mg/dL but ≥54 mg/dL)
• Level 2 (clinically significant): (<54 mg/dL).
• Level 3 (severe) is defined as any low blood glucose level
leading to cognitive impairment.
↑

6
 Treatment of Hypoglycemia

Level 1 & 2: Oral fast-acting carbohydrate (10–15 g) is taken

as glucose drink or Glucotabs
• 150–200 mL pure fruit juice
• 3–4 heaped teaspoons of sugar dissolved in water.
• Repeat capillary glucose measurement 1–15 mins later. or
Consider glucagon 1 mg IM or 150–200 mL 10% glucose over
15 mins IV.

Level 3: Intra venous dextrose over 15 minutes should be

given for semiconscious or unconscious patient
• Intra muscular glucagon injection
7
 Case
Hypoglycemia

8
An 18-year-old adolescent female is brought to the ER by
her mother because the daughter seems confused and is
behaving strangely.
The mother reports the patient has always been healthy
and has no significant medical history, but she has lost 20
lb recently without trying and has been complaining of
fatigue for 2 or 3 weeks.
The patient had attributed the fatigue to sleep
disturbance, as recently she has been getting up several
times at night to urinate. This morning, the mother found
the patient in her room, complaining of abdominal pain,
and she had vomited.
She appeared confused and did not know that today was
a school day.
9
On examination, the patient is slender, lying on a stretcher
with eyes closed, but she is responsive to questions.
She is afebrile, and has a heart rate 118 bpm, blood
pressure 125/84 mm Hg, with deep and rapid respiration
at the rate of 24 breaths per minute.
Upon standing, her heart rate rises to 145 bpm, and her
blood pressure falls to 110/80 mm Hg.
Her funduscopic examination is normal, her oral mucosa
is dry, and her neck veins are flat.
Her chest is clear to auscultation, and her heart is tachy-
cardiac with a regular rhythm and no murmur.
Her abdomen is soft with active bowel sounds and mild
diffuse tenderness, but no guarding or rebound. Her
neurologic
10
 Examination reveals no focal deficits
Laboratory studies include
• Na 131 mEq/L
• K 5.3 mEq/L
• Cl 95 mEq/L
• CO2 9 mEq/L
• BUN 35 mg/dL and creatinine 1.3 mg/dL
•
•
Glucose 475 mg/dL Loading…
pH 7.12 with PCO2 24 mm Hg and PO2 95 mm Hg
• Urine drug screen and urine pregnancy test are negative
• Urinalysis shows no hematuria or pyuria, but 3+ glucose and 3+
ketones.
Chest radiograph is read as normal, and plain film of the
abdomen has nonspecific gas pattern but no signs of
obstruction 11
I. What is the most likely diagnosis?
II. What is your next step?

12
 Overview
Precipitating Factors

• Infection (most common)

• MI, CVA and Pancreatitis
• Physiological Stress
• Insulin deficiency due to discontinuation or inadequate
delivery of insulin.
• Drug and social history may reveal glucocorticoid OR
cocaine use.

13
14
Clinical Features
Symptoms Signs

1. Polyuria 1. Dehydration

2. Thirst 2. Hypotension (postural or supine)

3. Weight loss 3. Cold extremities/peripheral cyanosis

4. Weakness 4. Tachycardia

5. Nausea, vomiting 5. Air hunger (Kussmaul’s breathing)

6. Leg cramps 6. Smell of acetone

7. Blurred vision 7. Hypothermia

8. Abdominal pain 8. Delirium, drowsiness, coma (10%)

15
 Investigations

• Urea
• Electrolytes, glucose
• Bicarbonate and acid–base status
• Hyponatremia and hyperkaliemia are common.
• Blood (or urine if unavailable) analysis for ketones
• Electrocardiogram (ECG)
• Chest X-ray
• Infection Screen
• Pregnancy test
16
Management
1- Fluid replacement
Time: 0–60 mins Time: 60 mins to 12 hrs Time: 12–24
hrs
If systolic BP > 90 IV infusion of 0.9% sodium chloride If patient is not
mmHg, give 1 L with potassium chloride added as eating and
over 60 mins indicated below : drinking

3
1 L over 2 hrs Continue IV fluid
1 L over 2 hrs replacement
1 L over 4 hrs and biochemical
1 L over 4 hrs monitoring
1 L over 6 hrs
If systolic BP < 90 change to 5% glucose and 0.45% saline (glucose saline )
mmHg, give 500 at 150–250 mL/h when plasma glucose reaches 250
mL over 10–15 mg/dL or continue NaCl and add 125 ml of GW 10% per 17
dextrose
 2- Insulin replacement

• A fixed-rate intravenous insulin infusion 0.1 U/kg body weight/hr

• Response to treatment should be assessed by a blood ketone
concentration falling by at least 0.5 mmol/L/hr.
• Aim for fall in blood glucose of 3-6 mmol/l(55-110 mg/dl)/hour
• A long-acting insulin analogue in a dose equivalent to the individual’s
usual regimen should continue to be administered subcutaneously
during the initial management of DKA.

18
 3- Potassium replacement

• Treatment with 0.9% sodium chloride with potassium chloride 40

mmol/L if the serum potassium is between 3.5 and 5.5 mmol/L and
there is no oliguria
• If potassium is >5.5 mmol/L then potassium is not added to fluid
replacement
• If potassium is <3.5 mmol/L at presentation then begin cardiac
monitoring.

4- Intravenous bicarbonate and phosphate

• Considered in the context of a pH of <6.9

19
 Additional Procedures in The Management of
Diabetic Ketoacidosis
• Catheterization if no urine passed after 3 hrs
• Nasogastric tube
• Central venous line
• Plasma expander if systolic BP is < 90 mmHg or does not rise with
I.V. saline
• Antibiotic if infection demonstrated or suspected
• ECG monitoring

20
 Chart for follow up

• Vital signs, RBS , blood ketone every hour

• Electrolyte every two hours
• ABG every 2-3 hours
• If blood ketone not fall at least 0.5 mmol/L/hr insulin dose
should be increased
Complications

1. cerebral oedema: Treated with oxygen & Mannitol

2. Acute respiratory distress syndrome
3. Thromboembolism
4. Disseminated intravascular coagulation
5. Acute circulatory failure 21
Hyperglycemic Hyperosmolar Nonketotic State
Pathophysiology

Relative insulin deficiency and inadequate fluid intake are the

underlying causes of HHS.
The reason for the absence of ketoacidosis in HHS is unknown.

Predisposing Factors
Chronic renal GI bleeding Gram-negative pneumonia
insufficiency
Gram-negative Sepsis Myocardial infarction 22
 Clinical features
Orthostatic hypotension or frank Thirst and initially polyuria then
hypotension oliguria
Signs of marked dehydration. Tachycardia
Fever Seizures
Decreased level of consciousness Coma
Differential Diagnoses
1. DKA
2. Chlorpropamide
3. Hypoglycemia 23
 HHS DKA
Geriatric population Younger
Typically type 2 diabetic patients Typically type 1 diabetic patients
Days to weeks Hours to days
Usually do not have metabolic acidosis Metabolic acidosis
Usually, absent N/V, abdominal pain and kussmaul
res.
Glucose (mg/dl) (600–1200) Dka (250–600)
Arterial PCO2, mmHg: normal 20–30 mmHg
Osmolality (mosm/ml) 330–380 300–320 24
 Treatment
Intravenous Fluids
hypovolemic shock: (0.9% normal saline over the first 2–3 h)
Hemodynamically stable: hypotonic fluids then 5% dextrose in
water
Insulin
IV insulin bolus of 0.1 unit/kg
IV insulin constant infusion rate of 0.1 unit/kg per hour
Electrolytes
Other considerations
• Phenytoin (Dilantin) is contraindicated for the seizures of HHS
• give low-dose subcutaneous heparin to lessen the risk of
thrombosis
25
 Thyroid Storm
An acute exacerbation of hyperthyroidism that results in a
life-threatening hypermetabolic state. Also known as
thyrotoxic crisis

Etiology
1. iatrogenic
• Thyroid surgery
• Exogenous iodine from contrast media or amiodarone
• Discontinuation of antithyroid medication
2. Stress-related catecholamine surge
3. Intercurrent illness
26
27
 Treatment

1. Should be rehydrated and given propranolol, either

orally (80 mg 4 times daily) or intravenously (1-5 mg 4
times daily)
2. Sodium ipodate (500 mg per day orally) will restore
serum t3 levels to normal in 48-72 hours
3. Dexamethasone (2 mg 4 times daily) and amiodarone
have similar effects
4. Oral carbimazole 40-60 mg daily
5. Acetaminophen and cooling blankets may be used to
control the hyperthermia
28
Myxedema Coma
Is Myxedema crisis is a severe life-threatening form of
decompensated hypothyroidism which is associated with a high
mortality rate
Etiologies
Loading…
Discontinuation of thyroid supplements Infections
Hypothermia Infections and septicemia
Cerebrovascular accidents Congestive heart failure
Gastrointestinal bleeding Drugs: anesthetics, sedatives,
tranquilizers, narcotics, amiodarone
and lithium 29
 Recognition of Myxedema Coma

• Patient profile
• Known hypothyroidism, thyroidectomy scar
• Hypothermia: maybe as low as 25c
• Altered mental status
• Hypotension: refractory to volume resuscitation and pressors
• Slow shallow respirations with hypercapnia and hypoxia
• Myxedema facies: puffy eyelids and lips, large tongue, broad
nose
• Evidence of severe chronic hypothyroidism or Acute
precipitating illness
• Drug toxicity
• Hyponatremia and hypoglycemia 30
 Picture of Patients
with Hypothyroidism

31
Investigations
1- Thyroid function test
2- Urea and electrolytes (Dilutional hyponatremia )
3- Random blood glucose (Hypoglycemia)
4- CBC and blood culture
5- ECG (Sinus Bradycardia)
6- Chest x-ray ( if there is pericardial effusion, pleura effusion)

32
 Treatment

• Treated with an IV injection of 20 µg liothyronine

• Followed by further injections of 20 µg 3 times daily until there
is sustained clinical improvement
• After 48-72 hours, it is usually possible to switch patients to oral
levothyroxine in a dose of 50 µg daily
• Treatment given with hydrocortisone 100mg I.M in secondary
hypothyroidism
• Other measures include slow rewarming, cautious use of IV
fluids, broad-spectrum antibiotics and high-flow O2

33
 Case scenario

A 37-year- old male presents to the ED with complaints of

palpitations, abdominal pain, nausea, vomiting, and
diaphoresis.
He reports episodes similar to this that have been increasing
in frequency and severity over several months.
His vital signs are P 127,BP 174/90 mmHg, RR 28, T 37.1°C,
and Sao2 96%. Once stabilized, what is the most appropriate
oral treatment for this patient?
a) Amlodipine 5 mg PO daily
by mouth
b) Metoprolol, 100 mg PO BID
c) Phenoxybenzamine 10 mg PO BID
d) Propranolol ER 80 mg PO daily. 34
 Pheochromocytomas
chromaffin cell
-
Overview &

-
-

The “rule of tens” for

pheochromocytomas states that about
• 10% are bilateral
• 10% are extra-adrenal,
• 10% are malignant

35
Clinical Features
Hypertension (usually paroxysmal; often Abdominal pain and
postural drop of blood pressure) vomiting
Constipation
Paroxysms of: Weight loss
• Pallor (occasionally flushing) Glucose intolerance
• Palpitations, sweating and headache
• Anxiety (angor animi)
Among the presenting symptoms, episodes of palpitations, headaches,
and profuse sweating are typical and constitute a classic triad. in
association with hypertension makes pheochromocytoma a likely
diagnosis
36
 urine-
>>
ng/2uh
plasma >
Tnoopglm/
=

Diagnosis
The diagnosis is based on
documentation of catecholamine
excess by biochemical testing (in
plasma and/or urine (Metanephrine
and normetanephrine). and
localization of the tumor by imaging.

37
 Management
• The most useful drug in the face of very high circulating
catecholamines is the α-blocker phenoxybenzamine (10–20
mg orally 3–4 times daily) non-competitive antigonist
• then a β-blocker such as propranolol can be added.
• Metastatic tumors: debulking surgery, radionuclide therapy

3
with 131I-MIBG, chemotherapy and (chemo) embolization of
hepatic metastases; some
- -may respond to tyrosine kinase
and =
-

angiogenesis inhibitors
-
y, %1d1;8 &900
s y5l
38
 Case scenario

A 52-year- old man is brought in by ambulance from his home with

altered mental status and hypotension. EMS reports that he
became ill with an influenza-like illness 4 days ago and stopped
taking all of his medications secondary to vomiting. Despite
multiple fluid boluses, he remains hypotensive. Laboratory results
demonstrate severe acidosis, hyponatremia and hyperkalemia.
What is the next step and most appropriate treatment for this
patient?
a) Adrenocorticotropic hormone (ACTH)
b) Continued normal saline (0.9%) fluid boluses
c) Hydrocortisone
d) Norepinephrine
39
 Adrenal Crisis

Pathophysiology and Classification

• Primary, secondary and tertiary
• Acute and chronic
• Adrenal crisis is usually seen in patients with Addison disease
because of mineralocorticoid deficiency but can also present in
patients with secondary or tertiary adrenal insufficiency who
undergo severe physiologic stress, or exogenous steroid
withdrawal.
Etiology
• Primary and acute: Adrenal hemorrhage
• Secondary or tertiary and acute: Postpartum pituitary necrosis,
Traumatic brain injury and exogenous steroid withdrawal. 40
 Clinical Features
• Adrenal crisis presents with hypotension (Refractory) and
shock that does not respond to fluid resuscitation and
pressors.
• Hypoglycemia
• Features of primary or secondary adrenal insufficiency
Diagnosis
• Hyponatremia
• Hyperkalemia
• Hypoglycemia
• Acidosis

41
 Treatment

• Treatment of adrenal crisis should begin as soon as possible

and prior to diagnostic testing when crisis is suspected
• Hemodynamically unstable: 0.9 NS, 2–3 L in the first few
hours with vasopressor
• Dexamethasone, 4 mg IV bolus or Hydrocortisone, 100 mg IV
bolus, followed by additional dosing of 200 mg/24 hrs as
bolus divided every 6 hrs or infusion if critically ill
• Switch to D5/NS if hypoglycemia
• Treat precipitating illness

42
 Case
Malignant Hypercalcaemia

43
 Malignant Hypercalcaemia
Hypercalcemia due to malignancy is common (20% of cancer patients)
Hypercalcemic crisis: levels higher than 14 mg/dL can be life-threatening
Pathophysiology
Parathyroid hormone-related protein (PTHrP) is the responsible humoral
agent in most solid tumors that cause hypercalcemia.
Tumors that produce and secrete PTHrP that causes increased bone
resorption
Etiologies
• Ectopic secretions of parathyroid hormone
• Multiple Myeloma
• Cancer metastatize to bone: Most common: Breast, lung, hematologic,
kidney, prostate

44
 Clinical Features
CNS: anxiety, depression, hallucinations, lethargy, altered mental status,
seizures, and coma
Cardiac Conduction Abnormalities: brady dysrhythmias (most
common) sinus arrest, AV block, AF and ventricular tachycardia.
Other Symptoms include: abdominal pain, constipation, fatigue, body
aches, anorexia, polydipsia, polyuria, nausea, and vomiting

Diagnosis
• Total serum calcium level: higher than 14 mg/dL
• Short QT interval
• ST segment elevation
• U waves in the precordial leads
45
 Treatment ‫ﻣﺎﻧﺴﺘﺨﺪم اﻟﺜﯿﺎزاﯾﺪ ﻻن اﺻﻼ ﯾﺰﯾﺪ اﻟﮭﺎﯾﺒﺮﻛﻼﯾﺴﯿﻤﺎ‬

• Hydration with normal saline

• Normal saline plus Loop Diuretic Furosemide after rehadation
• Osteoclast-inhibiting therapies: Bisphosphonates (Zoledronic
acid), calcitonin, and glucocorticoids.
• Denosumab: for persistent hypercalcemia despite
bisphosphonates therapy
• Hemodialysis: Last choice

46
 TAKE HOME NOTES

• Hypoglycemia, characterized by a plasma glucose level <70

mg/dL, can cause neuroglycopenic symptoms and
autonomic dysfunction. Prompt identification and treatment
with glucose or glucagon are crucial.
• Diabetic ketoacidosis (DKA) is a severe metabolic
complication of diabetes characterized by hyperglycemia,
ketonemia, and acidosis, requiring prompt treatment with
insulin, fluid resuscitation, and electrolyte management.

47
• Hyperglycemic hyperosmolar state (HHS) is a serious
diabetes complication characterized by extreme
hyperglycemia, high osmolarity, and dehydration without
significant ketone production, requiring urgent rehydration
and insulin therapy.

48
• Thyroid storm is a life-threatening exacerbation of
hyperthyroidism, marked by extreme thyrotoxicosis, fever,
tachycardia, and altered mental status. Prompt recognition
and treatment with antithyroid medications, beta-blockers,
and supportive care are crucial.
• Myxedema coma is a severe, life-threatening hypothyroid
emergency presenting with altered mental status,
hypothermia, and bradycardia, necessitating immediate
thyroid hormone replacement and intensive supportive care.

49
• Pheochromocytoma is a catecholamine-secreting tumor of
the adrenal gland causing episodic hypertension
(refractory to treatment), headache, and sweating.
• Diagnosis involves biochemical tests and imaging;
treatment is primarily surgical, with preoperative alpha-
blockade.

50
• Adrenal crisis is a life-threatening condition resulting from
acute adrenal insufficiency, characterized by refractory
hypotension, hypoglycemia, and electrolyte imbalances.
Prompt glucocorticoid administration is crucial.
• Malignant hypercalcemia, often a paraneoplastic
syndrome, results from cancer-induced increased calcium
release into the bloodstream, typically due to osteolytic
metastases or parathyroid hormone-related peptide.
Immediate management is crucial.

51
• Ron M. Walls - ROSEN'S EMERGENCY MEDICINE _ concepts and
clinical practice
• Harrison's Principles of Internal Medicine, 21st Edition
• Davidson’s Principles & Practice of Medicine 24rd edition 2022
• Amboss

52