ADRENAL CRISIS IN EMERGENCY MEDICINE DEPT

1. Adrenal Insufficiency
Dr ASHMAL
JR2,Emergency Medicine
GMC,KANNUR

2. TOPICS
• ANATOMY
• ADRENAL GLAND PHYSIOLOGY
• etiology
• CLINICAL FEATURES
• DIAGNOSIS
• TREATMENT
• DISPOSITION AND FOLLOW-UP

3. ANATOMY
• The adrenal glands are located on both sides of the body in
the retroperitoneum, above and slightly medial to the kidneys
• The adrenal glands (also known as suprarenal glands)
are endocrine glands that produce a variety of hormones
including adrenalineand the steroids aldosterone and cortisol.
• Each gland has an outer cortex which produces steroid
hormones and an inner medulla.
• The adrenal cortex itself is divided into three zones: the zona
glomerulosa, the zona fasciculata and the zona reticularis

5. •Mineralocorticoids (such as aldosterone)
produced in the zona glomerulosa help in the
regulation of blood pressure and electrolyte
balance
• The glucocorticoids cortisoland cortisone are
synthesized in the zona fasciculata; their
functions include the regulation
of metabolism and immune system suppression.
• The innermost layer of the cortex, the zona
reticularis, produces androgens that are
converted to fully functional sex hormones in
the gonads and other target organs.

6. ADRENAL GLAND PHYSIOLOGY
•Mineralocorticoids :
•In the kidneys, aldosterone acts on the distal convoluted
tubules and the collecting ducts by increasing the
reabsorption of Na and the excretion of both k+ and
hydrogen ions
•Angiotensin II and extracellular potassium are the two main
regulators of aldosterone production
•Aldosterone deficiency symptoms include dehydration,
syncope, salt craving, and hypotension

7. Glucocorticoids
•Cortisolis the main glucocorticoid in humans
•They increase the circulating level of glucose
Glucocorticoids also have effects unrelated to the regulation of
blood sugar levels, including the suppression of the immune
system and a potent anti inflammatory effect. Cortisol reduces
the capacity of osteoblasts to produce new bone tissue and
decreases the absorption of calcium in the gastrointestinal
tract.
•Secretion occurs in a diurnal rhythm, with higher levels
secreted in themorning and lower levels in the evening
•Regulate fat, glucose, protein metabolism

8. Catecholamines
• Adrenaline and noradrenaline act
at adrenoreceptors throughout the body
• Effects that include an increase in blood pressure
and heart rate.
•Actions of adrenaline and noradrenaline are
responsible for the fight or flight response
characterised by a quickening of breathing and heart
rate, an increase in blood pressure, and constriction
of blood vessels in many parts of the body.[32]

9. REGULATION
• Glucocorticoids are under the regulatory influence of
the hypothalamus-pituitary-adrenal (HPA) axis.
• Glucocorticoid synthesis is stimulated
by adrenocorticotropic hormone (ACTH), a hormone
released into the bloodstream by the anterior pituitary.
In turn, production of ACTH is stimulated by the
presence of corticotropin-releasing hormone(CRH),
which is released by neurons of the hypothalamus.
• Mineralocorticoid secretion is regulated mainly by
the renin–angiotensin–aldosterone system(RAAS), the
concentration of potassium, and to a lesser extent the
concentration of ACTH

10. Adrenal Insufficiency
1.Primary = failure of adrenal glands
2. Secondary = failure of HPA axis
– Usually due to chronic exogenous
glucocorticoid administration
_pituitary failure
•3. Tertiary = Hypothalamic dysfunction

11. PRIMARY ADRENAL INSUFFICIENCY
1.80% are due to an autoimmune disease called Addison's
disease or autoimmune adrenalitis
2.One subtype is called idiopathic
3.Other cases are due to congenital adrenal hyperplasia or
an adenoma (tumor) of the adrenal gland
TB = m.c. infectious cause worldwide

13. Addison's disease
• primary hypoadrenalism, which is a deficiency in glucocorticoid
and mineralocorticoid production by the adrenal gland.
•Addison's disease is most commonly an autoimmune condition
•. A distinctive feature of Addison'sdiseaseis hyperpigmentation of the
skin.
•Under certain circumstances, an adrenal crisis may occur with low
blood pressure, vomiting, lower back pain, and loss of consciousness.

14. SECONDARY ADRENAL INSUFFICIENCY:
Secondary adrenal insufficiency is caused by impairment of
the pituitary gland or hypothalamus.
HPA axis failure
– deficiency of glucocorticoids and adrenal androgens
– mineralcorticoids are unaffected
Less common causes
– Postpartum necrosis (Sheehan syndrome)
– Adenoma hemorrhage
– Pituitary destruction from head trauma
– typically have associated focal neurologicalchanges, visual deficits, diabetes
insipidus or panhypopituitarism

16. •Characterized by depressed adrenocorticotropic
hormone secretion, which reduces cortisol production,
butaldosterone levels remain normal because of
preserved stimulation byboth the renin-angiotensin
axis and potassium.
•Adrenal sex hormone production is also preserved.
•The most common cause of secondary adrenal
insufficiency is longterm
therapy with pharmacologic doses of glucocorticoids

17. Tertiary adrenal insufficiency:
Due to hypothalamic disease and a decrease in the
release of corticotropin releasing hormone (CRH)

19. •ADRENAL CRISIS
Optional statement
• Adrenal crisis is shock refractory to volume resuscitation and
pressors.
• It can result from acute destruction of the hypothalamic-pituitary
axis or the adrenal glands or from acute stressors in the setting of
underlying primary or secondary adrenal insufficiency.
•Life-threatening emergency
• Stressor : Acute infection, especially gastrointestinal infection;
surgery; extremephysical activity; acute severe injury or burns;
and cessation of chronic glucocorticoid replacement

20. Other symptoms include
severe abdominal pain, nausea,and vomiting, mimicking
an acute abdomen.
CNS symptoms of confusion,disorientation, and lethargy
.There may be associated sepsis, even without fever.
Consider adrenal crisis in situations of unexplainedhypotension,
especially in patients with a history of
glucocorticoidtherapy; those with acquired
immunodeficiency syndrome, tuberculosis,
autoimmune disease, or severe head trauma; those with a
history ofchronic fatigue and hyperpigmentation

21. LABORATORY STUDIES AND IMAGING
GRBS
CBC
Serum Electrolyte,ca, cortisol
LFT, RFT
ECG- POTTASIUM IMBALANCE
URINE ANALYSIS
CXR- TB,PNUEMONIA
CT ABDOMEN -TUMORS, ADRENAL GLAND HEMORRHAGE
HEAD CT / MRI- TUMORS

22. Primary adrenal insufficiency
Hyponatremiaand hyperkalemia due to aldosterone deficiency
High ACTH level
Low serum glucose
Low cortisol
Secondary adrenalinsufficiency
Low ACTH
LOW Cortisol
•serum cortisol>18 micrograms/dL generally rules out adrenal
insufficiency.
•ACTH stimulation test :250 microgram cosyntropin is given iv
if serum cortisol increases --- secondary

23. TREATMENT
• Primary adrenal insufficiency
• Daily dosing of glucocorticoidand mineralocorticoid, usually
for life.
• Androgen replacement may be recommended for women.
• The goal of treatment is to stabilize hormone levels and
relieve symptoms.
• Mineralocorticoids are replaced with an oral, synthetic
mineralocorticoid drug such as fludrocortisone The dose is
tailored to manage blood pressure and fluid balance.
• Secondary adrenalinsufficiency
• Only glucocorticoid replacement is required.
• Dose is 20 mg/day of oral hydrocortisone.
•Stress dose is three times daily dose

25. DISPOSITION AND FOLLOW UP
Admit patients with adrenal crisis to an intensive
care unit for careful clinical monitoring, IV steroid
administration, and confirmation of diagnosisand
identification of etiology.
Discharge can only be considered for mildcases of adrenal
insufficiency with identified etiologies and after a clear plan
of management is established.
Endocrinology consultation

26. PATIENTS ON CHRONIC CORTICOSTEROIDS
Hypothalamus-pituitary-adrenal axis function is inhibited with
chronic use of steroids. Always consider adrenal insufficiency in
patients with chronic steroid use presenting with any acute illness
PREGNANCY WITH ADRENAL INSUFFICIENCY
Most women with primary adrenal insufficiency are able to undergo
healthypregnancy, labor, and delivery.
Give hydrocortisone 100mg iv bolus during labour.
Dose adjustment may be needed

28. “Unexplained hyponatremia and
hyperkalemia in the setting of hypotension
unresponsive to catecholamine and fluid
administration… We should concider
ADRENAL CRISIS as an d/d in the emergency
medicie dept.
TAKE HOME MESSAGE !!