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Endocrinal emergencies. Dr. Miada Mahmoud Rady. Hyperosmolar Non ketotic coma. Also known as hyperglycemic , hyperosmolar ,Non ketotic coma ( HHNC). Occurs in neglected , uncontrolled diabetes esp. in elderly. Occurs primarily in type 2 diabetes .

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endocrinal emergencies

Endocrinal emergencies

Dr. Miada Mahmoud Rady

hyperosmolar non ketotic coma
Hyperosmolar Non ketotic coma
  • Also known as hyperglycemic , hyperosmolar ,Non ketotic coma ( HHNC).
  • Occurs in neglected , uncontrolled diabetes esp. in elderly.
  • Occurs primarily in type 2 diabetes .
  • Predisposing factor : stressful condition which impairs fluid intake e.g. infection , operation , stroke , MI .
slide3

Pathogenesis :

  • Stressful conditions → secretion of hormones that counteract effect the of insulin→ hyperglycemia.
  • Impaired ability to drink along with hyperglycemia causes hyperosmolarity.
  • Characterized by : hyperglycemia , hyperosmolarity and no significant ketosis.
slide4

Clinical presentation :

  • Symptoms of uncontrolled D.M
  • Sever dehydration.
  • Neurologic changes may be found, including:

i. Drowsiness.

ii. Delirium and coma

iii. Focal or generalized seizures

iv. Visual and sensory disturbances

v. Hemiparesis

Neurological symptoms occurs more with HONK

slide5

Stroke and MI can cause and result from HONK

  • Laboratory :
  • Hyperglycemia > 600 mg /dl.
  • Hyperosmolarity ( ↑Na conc.).
  • No ketosis.
  • Complication :
  • Increased blood viscosity which increase liability to cerebrovascular accident and myocardial infarction.
slide6

Management :

  • Airway management is the top priority.
  • Endotracheal intubation may be indicated for comatose patients.
  • Cervical spine immobilization should be used for all unresponsive patients found lying down.
  • Large-bore IV access should be gained as soon as possible.
slide7

Obtain a blood glucose level as soon as possible.

  • A bolus of 500 mL 0.9% NS is appropriate for nearly all adults who are clinically dehydrated.
  • In patients with a history of congestive heart failure and/or renal insufficiency, a 250-mL bolus may be more appropriate.
  • Administer 12.5 to 25 g of D50 if the glucose level is less than 60 to 80 mg/dL (depending on local protocols).
adrenal gland

4 s

Adrenal gland
  • located above kidney ( suprarenal gland ) .
  • Consists of two parts :
  • Hormones secreted and their function :
  • cortisol → sugar→ increase BMR using fat and protein for energy .
  • Aldestorone → salt → Na and water reabsorption (↑ Na ) , K excretion ( ↓ K ).
slide10

Androgens→ sex → sex hormones .

  • Adrenaline and noradrenaline → stress→ stimulates sympathetic nervous system .
  • Cortisol primary role is to assist with the response to stress, but it also:

a. Helps to maintain blood pressure and cardiovascular function

b. Regulates the metabolism of carbohydrates, proteins, and fats

c. Modulates glucose levels

d. Slows the inflammatory response

addison disease
Addison disease
  • Primary suprarenal failure
  • Etiology :decreased function of the adrenal cortex with decreased production of cortisol and aldestorone .
  • Pathophysiology : occurs when 90% of both glands are destroyed or atrophied .
  • Clinical presentation :
  • develops over several months
  • usually well tolerated
  • May present with Addison crises ( uncommon)
slide15

Management :

  • Address ABCS .
  • Aggressive fluid therapy.
    • Hydrocortisone is indicated in the acute management of a crisis.
secondary adrenal insufficiency
Secondary adrenal insufficiency
  • Pathophysiology :
    • lack of ACTH secretion from the pituitary gland
  • sudden withdrawal of corticosteroids in patient on chronic steroid therapy.
  • Presentation :
    • May appear suddenly (addisonian crisis)
    • Chief manifestation is shock
    • Symptoms may also include:
      • Confusion
      • Low blood pressure
      • Severe pain and/or vomiting
slide17

Management :

  • Address ABCS .
  • Aggressive fluid therapy.
    • Hydrocortisone is indicated in the acute management of a crisis.
cushing syndrome
Cushing syndrome
  • Pathophysiology :

Caused by:

  • Excess cortisol production by the adrenal glands :
  • Example: Tumors of the pituitary or adrenal cortex.
  • Excessive and prolonged use of cortisol or other corticosteroid hormones :
  • Example: treatment of asthma .
slide19

characteristic changes:

  • Metabolismof carbohydrate, protein, and fat is disturbed.

(a) Blood glucose level rises.

  • Protein synthesis is impaired.

(a) Body proteins are broken down.

  • Leads to loss of muscle fibers and muscle weakness.
  • Bones become weaker and more susceptible to fracture
signs and symptoms
signs and symptoms
  • Weakness and fatigue
  • Depression and mood swings
  • Increased thirst and urination
  • High blood glucose level
  • Weight gain

(a) Abdomen

(b) Face (“moon face”)

(c) Neck

(d) Upper back (“buffalo hump”)

slide21

Thinning of the skin

(a) Easy bruising

(b) Pink or purple stretch marks (striae)

  • Increased acne, facial hair growth, and scalp hair loss in women, and cessation of menstrual periods
  • Darkening of skin of the neck
  • Obesity and poor growth in height in children
management
Management
  • Assess and manage ABCs.
  • Prehospital treatment is generally supportive.
  • Obtain blood glucose level, and administer D50 if indicated.
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