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definition

causes

Risk factors

ADRENAL
CRISIS

pathophysiolo
gy

Managemen
t

manifestatio
ns

Diagnostic
and lab
exams

Addisonian Crisis
Also known as acute adrenal
insufficiency, may occur
when the client has been
under stress without
appropriate hormone
replacement.

Adrenocortical hormone
deficiency results in the
reverse of these hormonal
effects: glucocorticoids
(cortisol), mineralocorticoids
(aldosterone, 11deoxycorticosterone), and
androgens
(dehydroepiandrosterone).

Causes
Rapid withdrawal of long-term
steroid therapy
Direct injury to adrenal cortex
Rifampin
Septic shock

Risk Factors
Pregnancy
Surgery
Direct injury to adrenal cortex
Autoimmune diseases
Infection
States of dehydration or anorexia
Fever
Emotional upheaval

Manifestations
Abdominal pain
Confusion or coma
Darkening of the skin
Dehydration
Dizziness or lightheadedness
Fatigue
Flank pain

Headache
High fever
Joint pain
Loss of appetite
Loss of consciousness
Low blood pressure
Nausea
Profound weakness
Rapid heart rate

Rapid respiratory rate


Shaking chills
Skin rash or lesions
Slow, sluggish movement
Unintentional weight loss
Unusual and excessive
sweating on face or palms
Vomiting

Diagnostics and laboratory


exams
Serum chemistry
Serum cortisol
ACTH test
CBC
Serum thyroid levels
Serum thyroid levels

Chest radiography
Abdominal CT scanning

Pathophysiology
Predisposing
factors:
Autoimmune disease
Stressors
Excessive use/abrupt
withdrawal of
exogenous steroids
metastatic carcinoma
idiopathic
atrophy(most frequent
cause)

Adrenal exhaustion

Precipitating
factors:
Direct trauma to
adrenal cortex
Suppression of
hypothalamic
pituitary adrenal
axis
pituitary gland
injury

Destruction of the adrenal


gland function

Failure of adrenal glands to release


adequate amounts of hormones

Insufficient availability of
steroid hormones ( most
importantly the cortisol)

Adrenal crisis or
acute adrenal
insufficiency

Medications:
1.Glucocorticoids
. Hydrocortisone raises
adrenocorticoid hormonal levels. It is
administered intravenously. Restoration
of BP and general improvement should
occur within 1 h after the initial dose of
hydrocortisone.

2. MINERALOCORTICOID

Fludrocortisone (Florinef) - Acts on


renal distal tubules to enhance
reabsorption of sodium. Increases urinary
excretion of both potassium and
hydrogen ions. The consequence of these
3 primary effects, together with similar
actions on cation transport in other
tissues, appears to account for the
spectrum of physiological activities
characteristic of mineralocorticoids.
Produces marked sodium retention and
increased urinary potassium excretion.

3. VASOPRESSORS
Dopamine (Intropin) - Stimulates
both adrenergic and dopaminergic
receptors of the sympathetic NS thus
increase cardiac output and BP.
Hemodynamic effect is dependent on
the dose.

4. ANTIBIOTICS - may be administered if


infection has precipitated the occurrence of
adrenal crisis.

IV FLUIDS

1. D5 / D10 glucose for aggressive fluid


replacement and for Immediate
intravascular volume expansion.
2. 0.9% NSS for the treatment of
hypotension, dehydration, and
hyponatremia and for electrolyte
imbalances.

Assessment and Monitoring

Nursing
Interventions
1. Monitor vital signs especially BP Lying, sitting, and standing BP; a
decrease in systolic BP of 20 mmHg or
more indicate fluid volume depletion.

Monitor neurological status, noting irritability and confusion.

2. Assess skin turgor, mucous


membranes, weight; report increased
thirst indicates impending fluid
imbalance.

3. Monitor neurological status, noting


irritability and confusion.

4. Monitor intake and output.

5. Monitor laboratory values


sodium, potassium, and blood
glucose.

6. Prevent infection - Avoid exposure


to chickenpox or measles and other
infectious diseases; if exposed, seek
medical advice without delay.

7. Bed rest and quiet environment Until condition is stable, take


precautions to avoid unnecessary
activity and stress that could
precipitate hypotensive episode.
During acute crisis, maintain a quiet,
nonstressful environment and
performs all activities for the patient.

END
Prepared by:
Mitchell Fuertes
Gladys Dorilag
Wenna Rose Dongor
Jo Hiola
BSN 4A