This document outlines the causes, clinical features, diagnosis, and management of an Addisonian crisis, which is a life-threatening adrenal insufficiency emergency. It may be triggered by stress, infection, trauma, or withdrawal from steroids. Symptoms include nausea, vomiting, abdominal pain, hypotension, and electrolyte imbalances. Treatment involves intravenous hydrocortisone, fluids, glucose, and identifying and treating any precipitating causes. Long term management consists of glucocorticoid and mineralocorticoid replacement therapy and patient education.

1. ADDISONIAN CRISIS

2. OUTLINE
• INTRODUCTION
• ADRENAL FUNCTION
• CAUSES
• CLINICAL FEATURES
• DIAGNOSIS
• MANAGEMENT

3. • Life-threatening emergency Triggered by anything that increases the
person’s normal stress level The body is unable to release sufficient
cortisol to respond appropriately May lead to shock & vascular
collapse Typically resistant to catecholamine and IVF resuscitation

4. • The Adrenal Gland releases… Androgens (sex hormones)
Mineralocorticoids Glucocorticoids Glucocortoicoids (most potent is
cortisol) Action: anti-inflammatory, growth suppressing, affects sleep
patterns & awareness, stress response Mineralcorticoids
(Aldosterone) Action: Manages sodium/potassium balance Internet.

5. • Dehydration, hypotension, or shock out of proportion to severity of
current illness Nausea and vomiting with a history of weight lost
and anorexia Abdominal pain, so-called acute abdomen
Unexplained hypoglycemia Unexplained fever Hyponatremia,
hyperkalemia, azotemia, hypercalcemia, or eosinophilia
Hyperpigmentation or vitiligo Other autoimmune endocrine
deficiencies, such as hypothyroidism or gonadal failure Kronenberg -

6. • Abrupt adrenal failure usually from Bilateral adrenal infarction
Bilateral adrenal Hemorrhage Primary Adrenal Insufficiency
Serious infection Acute stress in previously undiagnosed cases No
extra glucocorticoid therapy during infection Secondary
adrenocortical insufficiency -Abrupt withdrawal from glucocorticoids
Catastrophic HPA axis failure Head trauma Hemorrhage of
pituitary adenoma Post-partum herniation (Sheehan syndrome)

7. • mmediate Laboratory Work up Electrolytes, glucose Baseline
Cortisol and ACTH Send immediately (before steroid administration)
Send in early morning sample if pt is stable with suspected chronic
adrenal insufficiency Can measure urinary 17-OHCS Renin(+/-
aldosterone- less sensitive)Random Cortisol

8. • Cosyntropin(synthetic ACTH) stimulation test is (used in all patients in
whom adrenal insufficiency is being considered Cortisol levels
measured at 0 and 30 minutes following cosyntropin administration
Normal response is defined by a peak plasma cortisol of > 20mcg/dl.
Primary adrenal insufficiency has a low or no rise in cortisol
following ACTH stimulation Secondary or Tertiary causes due to
deficient endogenous ACTH have an increase in cortisol (sub sub-
normal) following ACTH stimulation

9. • Imaging: Abdominal CT to evaluate for adrenal findings (ie.
Infection, calcification, hemorrhage) Head CT or MRI if secondary AI
is diagnosed Other Labs: Anti-adrenal antibodies VLCFA (very
long chain fatty acids)(acids) Especially in young males with negative
antibodies Evaluate for other autoimmune disorders as indicated
PPD if TB is suspected Metyrapone test: : ↓↓cortisol synthesis,
should see a resultant ↑↑in ACTH. Used to diagnosis partial ACTH

10. • EMERGENCY MEASURES 1) Establish intravenous access with a large-
gauge needle 2) Draw blood for stat serum electrolytes and glucose
and routine measurement of plasma cortisol and ACTH. Do not wait
for laboratory results. 3) Infuse 2 to 3 L of 0.9% saline solution or 5%
dextrose in 0.9% saline solution as quickly as possible. Monitor for
signs of fluid overload by measuring central or peripheral venous
pressure and listening for pulmonary rales. Reduce infusion rate if
indicated. 4) Inject intravenous hydrocortisone (100 mg immediately
and every 6 hr) 5) Use supportive measures as needed

11. • Continue iv 0.9% saline solution at a slower rate for next 24 to 48 hr
Search for and treat possible infectious precipitating causes of the
adrenal crisis Perform a short ACTH stimulation test to confirm the
diagnosis of adrenal insufficiency, if he is not a known case .
Determine the type of adrenal insufficiency and its cause if not
already known. Taper glucocorticoids to maintenance dosage over 1
to 3 days, if precipitating or complicating illness permits. Begin
mineralocorticoid replacement with fludrocortisone (0.1 mg by
mouth daily) when saline infusion is stopped.

12. • Glucocorticoid replacement Dexamethasone or prednisone (longer-
acting or once daily acting) daily Alternative therapy with
hydrocortisone BID -TID Mineralocorticoid replacement
Fludrocortisone Liberal salt intake Patient Education Recognition
and treatment of minor and major stress/ illness Instructions to
triple the dose of steroid in the event of an intercurrent illness,
accident or mental stress Emergency precautions Medic-alert
bracelet, pre alert pre--filled dexamethasone syringes

13. • Tuberculosis is known to affect adrenal glands directly. Adrenal
destruction by tuberculosis may lead to overt or subclinical adrenal
insufficiency In India it is the most common cause of Addison’s
disease . CT abdomen shows typically shrunken and calcified
adrenals in chronic stage and enlarged in the active stage. Confirmed
by FNAC ATT increase the degratdation of corticosteroids, may
precipitate the adrenal crisis & has been reported with rifampicin
therapy

14. • Causes of Addison’s crisisCauses of Addison’s crisis Stress; Infection;
Septic shock ; Rapid withdrawal of long-term steroid therapy Trauma;
Surgery; Emotional turmoil; Bilateral adrenal hemorrhage –
Waterhouse-Friderichsen syndromeWaterhouse-Friderichsen
syndrome (a complication of bacterial infection with Meningococcus
or Pseudomonas species); Bilateral adrenal artery emboli and bilateral
vein thrombosis; Bilateral adrenalectomy for any reason

15. • PATHWAY OF ADDISON’S CRISISPATHWAY OF ADDISON’S CRISIS
CortisolCortisol (hydrocortisone,(hydrocortisone, cortisone
acetate,cortisone acetate, prednosolone orprednosolone or
dexamethasone)dexamethasone) very lowvery low or absentor absent
Liver functionLiver function decreasesdecreases Mild or moderateMild or
moderate hypoglycemiahypoglycemia SevereSevere
hypoglycemiahypoglycemia Brain comaBrain coma andand
deathdeathAdrenal glands not functioning Stomach digestiveStomach
digestive enzymes decreaseenzymes decrease Vomiting Diarrhea Cramps
ShockShock AldosteroneAldosterone (Florinet) very low(Florinet) very low
or absentor absent Kidney-waterKidney-water and sodiumand sodium
lossloss Heart irregular andHeart irregular and output decreasesoutput
decreases Low fluid volume Low blood pressure

16. • Waterhouse-Friderichsen syndromeWaterhouse-Friderichsen
syndrome MeningococcemiaMeningococcemia Apoplexy ofApoplexy
of adrenaladrenal glandsglands Vascular collapseVascular collapse
Hyperthermia – 40,5Hyperthermia – 40,5° C° C or higheror higher
AbdominalAbdominal symptoms:symptoms: Nausea Vomiting Shock
and appear cyanotic oand oconfused

17. • FIRST AID OF ADDISON’S CRISISFIRST AID OF ADDISON’S CRISIS
I.Glucocorticoid therapy:I.Glucocorticoid therapy:
HydrocortisoneHydrocortisone 100 mg100 mg intravenous (i/v)) +
400 ml of 5 % solution glucose+ 400 ml of 5 % solution glucose and
100 mg hydrocortisoneand 100 mg hydrocortisone i/mi/m every 4 – 6
hours;every 4 – 6 hours; HydrocortisoneHydrocortisone 50-100 mg
i/v50-100 mg i/v (i/m)(i/m) every 6 hours.every 6 hours. Under
unstableUnder unstable condition or complications the
hydrocortisonehydrocortisone dose should be increased to 200-400
mg per day.200-400 mg per day.

18. • At a stable hemodynamicsAt a stable hemodynamics::
HydrocortisoneHydrocortisone 25 mg i/m q.d.25 mg i/m q.d. (15-20 mg in
the morning and 10 mg at 16-17 hours, it is possible per os)
PrednisonePrednisone 5-7.5 mg p/o5-7.5 mg p/o q.d in a.m.q.d in a.m.
FludrocortisoneFludrocortisone 0.1-0.2 mg p/o0.1-0.2 mg p/o q.d.q.d.
II.General arrangementsII.General arrangements Correction of
electrolytes Rehydration (0.9% NaCl0.9% NaCl solutionsolution 30 – 40
ml /kg30 – 40 ml /kg) Hypoglycemia liquidation (i/v injection of 0.9%
NaCli/v injection of 0.9% NaCl solution, 5% glucose solutionsolution, 5%
glucose solution) Correction of hypotension (Deoxycorticosterone
acetateDeoxycorticosterone acetate 0.5 % - 1 – 2 ml i/m0.5 % - 1 – 2 ml i/m
subcutaneous injection of 0.1 % -1.0 ml adrenaline0.1 % -1.0 ml adrenaline
or 0.2 % - 1.0-2.0 ml0.2 % - 1.0-2.0 ml noradrenalinenoradrenaline)) At
unrestrained vomiting: 10 % - 10 ml NaCl solutionNaCl solution i/v q.d.
Symptomatic therapySymptomatic therapy (Antibiotic et)

19. • Causes: • Sudden withdrawal of steroid(commonest cause, if pt. on
steroid for long time) • Following stress e.g.intercurrent
disease,trauma, surgery, severe infection or prolonged fasting in a pt
with latent insufficiency • Following sudden destruction of pituitary
gland(pituitary necrosis)or when thyroid hormone or drugs which
increase steroid metabolism(e.g. phenytoin)given to a pt with
hypoadrenalism • Following bilateral adrenalectomy • Following
injury to both adrenals due to trauma,adrenal vein
thrombosis,adrenal haemorrhage due to meningococcaemia or
anticoagulant therapy

20. • Clinical Features: • Nausea, vomiting, diarrhoea • Abdominal pain •
Diarrhoea • Muscle cramps • Unexplained fever • Unconsciousness •
Severe hypotension • Hyponatraemia, hyperkalaemia, hypoglycaemia,
hypercalcaemia

21. • Treatment: • I/V hydrocortisone 100 mg 6 hrly until GI symptoms
abate then oral therapy • I/V fluid normal saline and 10% dextrose for
hypoglycaemia • Precipitating factors should be find out and treated