Clinical Guides
Acute Adrenal Insufficiency (Adrenal Crisis)
A clinically focused emergency guide to recognising suspected adrenal crisis, giving immediate hydrocortisone and fluids without waiting for tests, treating the precipitant, and preventing recurrence through practical sick-day planning in India.
MedNext Academy | 13 min read
Acute Adrenal Insufficiency (Adrenal Crisis)
A clinically focused emergency guide to recognising suspected adrenal crisis, giving immediate hydrocortisone and fluids without waiting for tests, treating the precipitant, and preventing recurrence through practical sick-day planning in India.
Summary
Adrenal crisis is life-threatening acute cortisol deficiency causing circulatory and metabolic decompensation. It may occur in known primary or secondary adrenal insufficiency, after interruption of chronic glucocorticoids, or as the first presentation of previously unrecognised disease. Hypotension or shock, severe weakness, vomiting, abdominal pain, fever, confusion, hyponatraemia or hypoglycaemia should trigger suspicion, especially with steroid exposure, pituitary disease, autoimmune illness, tuberculosis, bilateral adrenal disease or recent physiological stress. Hyperkalaemia supports primary adrenal failure but may be absent; its absence never excludes crisis.
Treatment is clinical and time-critical. Give hydrocortisone 100 mg intravenously or intramuscularly immediately in an adult with suspected crisis, then provide 200 mg over 24 hours by continuous infusion or 50 mg every six hours under the receiving protocol. Begin rapid isotonic saline, reassessing for age, cardiac or renal impairment, and give glucose when hypoglycaemia is present. Draw cortisol and adrenocorticotropic hormone (ACTH) before steroid only if this causes no delay. Short-term hydrocortisone is far safer than withholding it from a shocked patient.
Search for and treat the precipitant while monitoring blood pressure, glucose, sodium, potassium, renal function and fluid balance. Specialist advice guides taper to oral replacement and investigation of the underlying cause after recovery. Discharge requires an emergency steroid card, sick-day dosing instructions, an injection kit with training where appropriate, reliable medication access and early endocrine follow-up. This quarantined draft supports supervised education and is has been reviewed by the MedNext Clinical Team.
How Common Is It?
Adrenal insufficiency is uncommon, and adrenal crisis is an infrequent but recurrent emergency within that population. Rates differ by case definition, underlying primary or secondary disease, glucocorticoid exposure, patient education and healthcare access. Prospective and registry studies cited by endocrine guidance show that people with established adrenal insufficiency remain at measurable annual risk despite replacement therapy, but those estimates should not be converted into a national Indian incidence. First presentations are easily missed because vomiting, fever, abdominal pain, hyponatraemia and shock overlap with sepsis and gastrointestinal illness.
Risk continues after diagnosis. Previous crisis, infection, gastrointestinal illness that prevents tablet absorption, failure to increase glucocorticoid during stress, surgery without adequate cover and interruption of steroid supply are recurrent patterns. Children and adults with congenital adrenal hyperplasia, people with autoimmune primary disease, pituitary disorders and patients exposed to long-term systemic glucocorticoids form different populations. Oncology immunotherapies add an evolving iatrogenic group.
India has no single comprehensive dataset spanning public emergency departments, rural facilities, endocrine centres and private hospitals. Tuberculosis-related adrenal damage, access to diagnostic testing, continuity of replacement medicines and patient-held emergency information may influence burden, but their contribution must be measured rather than asserted. Local audit should capture time from triage to hydrocortisone, fluid initiation, glucose correction, identified precipitant, prior steroid history, mortality, readmission and whether prevention equipment and education were actually supplied before discharge.
Risk Factors
Established primary adrenal insufficiency carries crisis risk during fever, gastroenteritis, trauma, surgery, labour or another major stress if glucocorticoid is not increased or cannot be absorbed. Autoimmune adrenalitis is a common cause internationally; in India, tuberculosis, adrenal haemorrhage, infiltration, infection and prior adrenal surgery also deserve history-based consideration. People with congenital adrenal hyperplasia or genetic adrenal disorders may decompensate. Mineralocorticoid deficiency in primary disease worsens sodium loss, potassium retention and volume depletion.
Secondary or tertiary adrenal insufficiency follows pituitary or hypothalamic disease, surgery, irradiation, apoplexy, traumatic brain injury or suppression of the hypothalamic-pituitary-adrenal axis by exogenous glucocorticoids. Risk depends on dose, potency, route, duration and individual susceptibility; oral, injected, inhaled, topical and intra-articular exposure can combine. Abrupt cessation after prolonged treatment, failure to disclose steroid use, or perioperative omission can precipitate crisis. Immune checkpoint inhibitors may cause hypophysitis or primary adrenal damage.
Common precipitants are vomiting or diarrhoea, respiratory or urinary infection, sepsis, surgery, dental procedures, trauma and intense physical stress. A patient who cannot retain oral steroid has a delivery failure even if they know sick-day rules. Additional vulnerability comes from previous crisis, absent injection training, no emergency card, language barriers, travel, medication stock-outs and delayed transfer. Enzyme-inducing medicines can alter steroid exposure. Ask about traditional or unlabelled products that may contain corticosteroid, but do not assume they do. Prevention targets both physiology and access.
Diagnosis
History
Ask immediately about known Addison disease or pituitary disease, usual glucocorticoid and fludrocortisone, last retained dose, recent dose reduction, vomiting, diarrhoea, fever, infection symptoms, surgery, trauma, pregnancy and prior crisis. Reconstruct all steroid exposure, including tablets, injections, inhalers, creams and traditional preparations. Symptoms include profound weakness, dizziness, anorexia, nausea, abdominal or back pain, salt craving, confusion and collapse. Hyperpigmentation and weight loss suggest chronic primary disease but may be absent.
Examination
Prioritise airway, breathing, circulation, mental state, temperature, capillary glucose and shock signs. Measure lying and standing blood pressure only when safe. Look for dehydration, hyperpigmentation, vitiligo, abdominal tenderness, infection, meningism, purpura, pituitary visual signs and evidence of trauma or haemorrhage. Primary adrenal crisis can resemble an acute abdomen. Secondary disease usually lacks hyperpigmentation and hyperkalaemia.
Investigations
Obtain electrolytes, urea, creatinine, glucose, full blood count, liver tests, calcium, blood gas and cultures or imaging directed by the precipitant. Save serum cortisol and plasma ACTH before hydrocortisone only when immediately available and treatment is not delayed. Renin and aldosterone, paired ACTH-cortisol interpretation, short Synacthen testing and aetiological imaging belong after stabilisation. A low random cortisol during severe stress may support adrenal failure, but assay, binding proteins and prior steroid complicate thresholds. Hyponatraemia, hyperkalaemia, hypoglycaemia, eosinophilia and prerenal kidney injury support the diagnosis; none is individually required.
Differential Diagnosis
Septic shock is the major parallel diagnosis and may also precipitate adrenal crisis. Do not force an either-or choice: obtain cultures and give indicated antimicrobials and source control while treating suspected cortisol deficiency. Hypovolaemic, haemorrhagic, cardiogenic, obstructive and anaphylactic shock require physiology-directed assessment. Persistent hypotension despite fluids and vasopressors, unexplained hyponatraemia or a steroid history should increase suspicion, but response to hydrocortisone alone is not a retrospective diagnostic test.
Gastroenteritis, pancreatitis, perforation, obstruction, hepatitis and other abdominal emergencies can produce vomiting, pain and dehydration. Adrenal crisis itself can cause marked abdominal tenderness, yet focal peritonism, bleeding or persistent pain after resuscitation needs imaging and surgical review. Hypoglycaemia may arise from insulin or sulfonylureas, liver failure, sepsis, alcohol or malnutrition. Severe hypothyroidism, pituitary apoplexy, salt-losing nephropathy, cerebral salt wasting and syndrome of inappropriate antidiuresis enter the hyponatraemia differential.
Primary and secondary adrenal insufficiency must later be separated. Primary disease has deficient cortisol and often aldosterone with raised ACTH; secondary disease has deficient ACTH, usually preserved aldosterone and possible other pituitary deficits. Hyperkalaemia can instead reflect acute kidney injury, acidosis, medicines or sample haemolysis. Waterhouse-Friderichsen syndrome, bilateral adrenal haemorrhage, tuberculosis, HIV-related infection and metastatic infiltration are cause-specific considerations. Thyroxine started before glucocorticoid in combined pituitary or autoimmune disease can worsen decompensation, so suspected cortisol deficiency takes priority.
Management
Treat on suspicion. Give adult hydrocortisone 100 mg IV or IM immediately; do not wait for cortisol, ACTH, imaging or endocrine review. Continue 200 mg hydrocortisone per 24 hours by continuous IV infusion or 50 mg IV or IM every six hours according to the emergency protocol. Establish venous access, cardiac and oxygen monitoring as indicated, check capillary glucose and begin isotonic saline. current guidelines (2024) recommends 1 litre of 0.9% sodium chloride over 30 minutes for an adult crisis, followed by further fluid guided by haemodynamics, urine output, sodium, age and cardiac or renal status. Give IV glucose for hypoglycaemia and recheck frequently.
Reassess rather than prescribing a fixed fluid total. Monitor blood pressure, pulse, temperature, mental state, oxygenation, input-output, glucose, sodium, potassium and creatinine. Severe hyponatraemia is usually corrected through steroid and volume treatment; avoid overly rapid sodium correction and seek specialist help when chronicity or neurological symptoms create osmotic risk. Vasopressors may be required in refractory shock after adequate resuscitation. High-dose hydrocortisone supplies sufficient mineralocorticoid activity initially, so additional fludrocortisone is generally introduced when hydrocortisone falls below stress doses in primary disease.
Identify and treat the trigger: cultures and antimicrobials for suspected infection, surgery or haemorrhage pathways where indicated, and correction of missed or malabsorbed steroid. Once stable and able to eat and drink, endocrine advice guides taper to oral replacement, usually over one to three days depending on illness. Document the provisional cause, tests saved before treatment, and a prevention plan; biochemical improvement without restored steroid access is incomplete care.
Prescribing Information
Hydrocortisone is preferred because it replaces glucocorticoid rapidly and, at stress doses, has useful mineralocorticoid activity. In an adult crisis, 100 mg parenteral hydrocortisone is an emergency dose, not a test dose. Follow with 200 mg over 24 hours or 50 mg every six hours. Confirm the formulation, reconstitution, route, administration time and ongoing prescription; a first dose given in ambulance or clinic can be lost during transfer unless it is handed over. If IV access is delayed, IM administration is appropriate. Pregnancy is not a reason to withhold life-saving hydrocortisone.
Isotonic crystalloid is also a prescription. Give rapidly for shock, but use smaller reassessed aliquots in older patients or those with heart or kidney failure. Hypoglycaemia requires glucose, with concentration and route adapted to consciousness and venous access. Potassium replacement is not routine in untreated primary crisis because potassium may be high; repeat measurements after fluid and steroid, exclude haemolysis and treat dangerous hyperkalaemia through an emergency pathway. Antimicrobials are guided by the suspected source and local resistance policy.
During recovery, oral hydrocortisone or another specialist-selected glucocorticoid is divided to approximate circadian physiology. Fludrocortisone is required for most primary adrenal insufficiency once hydrocortisone is below high stress doses; it is usually unnecessary in secondary disease. Never stop chronic glucocorticoid abruptly. Provide sufficient tablets, a written sick-day plan, a steroid emergency card and, when indicated, injectable hydrocortisone with needles, diluent and hands-on training. Product strengths and kit availability vary in India, so discharge teaching must match the supplied preparation.
When to Refer
Suspected adrenal crisis belongs in an emergency department or monitored acute-care setting. Call senior emergency or critical-care support for shock, reduced consciousness, severe hypoglycaemia, major electrolyte disturbance, arrhythmia, sepsis, pregnancy, adrenal haemorrhage, pituitary apoplexy or failure to improve promptly after hydrocortisone and fluids. Transfer from a facility without monitoring or parenteral steroid should start early, but give hydrocortisone and initial fluid before transport when possible. No referral conversation should delay the first dose.
Endocrinology should review every new or recurrent crisis to confirm primary versus secondary disease, plan definitive testing, assess mineralocorticoid need and investigate autoimmune, pituitary, infective, haemorrhagic, genetic or iatrogenic causes. Involve infectious diseases or respiratory medicine for tuberculosis or complex infection; neurosurgery and ophthalmology for pituitary apoplexy; obstetric medicine in pregnancy; and haematology, surgery or interventional radiology for bilateral haemorrhage or another structural emergency. Paediatric patients require weight-based paediatric protocols.
The referral must state steroid doses and exact times, fluid given, glucose treatment, serial observations, sodium and potassium trends, prior steroid exposure, pregnancy status and suspected precipitant. Include any cortisol and ACTH specimen time relative to hydrocortisone. At discharge, refer for early endocrine follow-up and primary-care medication reconciliation. A patient without affordable replacement, an emergency card, injection access or someone trained to help remains at preventable risk and should not be treated as administratively complete.
Red Flags
Hypotension, syncope, altered consciousness, seizure, severe weakness, persistent vomiting, hypoglycaemia, rapidly falling sodium or hyperkalaemia with ECG change demands immediate treatment. Purpura, meningism, high fever or rapidly progressive shock raises fulminant infection and possible bilateral adrenal haemorrhage. Sudden severe headache, visual loss, ophthalmoplegia or collapse suggests pituitary apoplexy. Abdominal or flank pain with anticoagulation, trauma, sepsis or antiphospholipid disease should prompt consideration of adrenal haemorrhage. These findings require parallel emergency pathways, not observation for a cortisol result.
A normal potassium does not reassure because secondary adrenal insufficiency preserves aldosterone, and vomiting or prior fluid can alter values. A normal blood pressure early in illness does not exclude impending crisis. Conversely, hyponatraemia alone is not proof; giving fluid or hydrocortisone should be accompanied by diagnostic reassessment. Watch sodium correction, fluid overload, pulmonary oedema and hyperglycaemia during treatment, particularly in older adults, CKD or heart failure.
System failures are red flags too: no hydrocortisone in the emergency trolley, an expired injection kit, a steroid card ignored at triage, an undocumented pre-transfer dose, or a patient discharged after vomiting without a parenteral backup. Recurrent crisis suggests that the education or access plan has failed, not merely that the patient was non-adherent. Before oral transition, confirm vomiting has stopped and tablets are retained. Before discharge, use teach-back for sick-day actions and verify the exact supplied medicine and emergency destination.
Indian Clinical Context
In India, adrenal crisis may first present to a primary health centre, small hospital or emergency unit without rapid cortisol testing. The safe minimum is clinical recognition, capillary glucose, electrolytes where available, immediate parenteral hydrocortisone, initial isotonic fluid and organised transfer. Hydrocortisone should not be withheld because ACTH, Synacthen testing, CT or an endocrinologist is unavailable. The referral note must preserve times, because later interpretation depends on whether blood was drawn before or after steroid.
Tuberculosis remains an important cause of primary adrenal destruction, but a past infection or positive test does not establish adrenal involvement. Evaluate constitutional symptoms, imaging and microbiology after stabilisation. Autoimmune disease, pituitary tumours, postpartum pituitary injury, exogenous steroid suppression, bilateral haemorrhage, HIV-related infection and metastatic disease also occur. Over-the-counter, injected, inhaled, dermatological and traditional preparations may contain glucocorticoid; ask non-judgmentally and inspect packaging. Abrupt shortage or withdrawal can be the precipitant.
Emergency injection kits and branded steroid cards are not uniformly available. Services should provide a locally understandable written card stating diagnosis, usual medicine, emergency hydrocortisone dose and contact number, and teach a family member when consented. Patients travelling between states need generic names, doses and a reserve supply. Sick-day teaching must account for heat, fasting, vomiting, literacy and distance to care. Evidence on Indian crisis incidence and prevention delivery is limited, so institutions should audit stock, time-to-steroid, recurrent admissions and actual kit competence rather than assume counselling was effective.
NMC Competency Mapping
Acute adrenal insufficiency integrates endocrine physiology, electrolyte and glucose interpretation, shock resuscitation, infectious and pituitary differentials, pharmacology of corticosteroids and communication for chronic disease safety. The NMC 2024 curriculum should be linked through the locally verified General Medicine emergency, endocrine, pharmacology and integrated teaching competencies. Because competency numbering may differ across curriculum compendia, this draft does not invent a code; faculty should bind it to the approved institutional ledger and document the level of supervision expected.
The learner should recognise a crisis phenotype, obtain a complete steroid history, distinguish primary from secondary biochemical patterns, and explain why cortisol and ACTH sampling must never delay hydrocortisone. They should state the adult emergency sequence: ABC assessment, glucose, immediate 100 mg IV or IM hydrocortisone, isotonic fluid, ongoing stress-dose steroid, monitoring and precipitant treatment. They should understand that hyperkalaemia is not obligatory and that sepsis and adrenal crisis can coexist.
A simulation can assess preparation and administration of an emergency hydrocortisone dose, fluid prescription with comorbidity adjustment, timed handover and escalation. Communication assessment should include sick-day teach-back, vomiting actions, emergency card use and injection-kit demonstration. Independent diagnosis, tapering and long-term mineralocorticoid adjustment require supervised clinical practice and endocrine review. This reviewed draft is educational and has been reviewed by the MedNext Clinical Team; it does not replace a hospital's emergency drug chart or confer prescribing authority.
Key Exam Pearls for NEET PG
Primary adrenal insufficiency causes low cortisol, high ACTH and often low aldosterone, producing hyperpigmentation, postural hypotension, hyponatraemia and hyperkalaemia. Secondary disease causes low cortisol with low or inappropriately normal ACTH; aldosterone is usually preserved, so hyperkalaemia and salt craving may be absent. Both can cause hypoglycaemia, weakness and shock. Eosinophilia may be a clue, not a diagnostic requirement. In critical illness, interpret cortisol with assay and timing, but never delay emergency steroid for a confirmatory threshold.
The adult crisis dose is hydrocortisone 100 mg IV or IM immediately, followed by 200 mg in 24 hours or 50 mg every six hours, plus isotonic saline and glucose when needed. High-dose hydrocortisone provides enough mineralocorticoid effect initially. Fludrocortisone becomes relevant in primary disease as hydrocortisone returns below stress dosing. Correct the precipitant and monitor glucose, sodium, potassium, renal function and haemodynamics.
Vomiting after oral replacement means the dose may not be absorbed. Sick-day rules increase oral glucocorticoid during febrile illness, while persistent vomiting, severe weakness, collapse or inability to retain tablets requires injected steroid and emergency care. Steroid treatment before thyroxine is the safe sequence when combined pituitary failure is possible. Pituitary apoplexy causes sudden headache and visual or ocular-motor signs; Waterhouse-Friderichsen syndrome causes sepsis, purpura and adrenal haemorrhage. Never stop long-term glucocorticoid abruptly.
Frequently Asked Questions
Should hydrocortisone wait until cortisol and ACTH results are available?
No. In suspected adrenal crisis, give hydrocortisone immediately. A cortisol and ACTH sample can be drawn first only if it is instantly available and causes no treatment delay. Record the sampling and steroid times for later interpretation. Short-term emergency hydrocortisone is unlikely to harm a patient without adrenal insufficiency, whereas delayed treatment can be fatal.
Can adrenal crisis occur without hyperkalaemia or hyperpigmentation?
Yes. Secondary adrenal insufficiency usually preserves aldosterone, so potassium may be normal and hyperpigmentation is absent. Vomiting, prior fluids or other medicines can also alter potassium in primary disease. Suspect crisis from the whole picture: steroid or pituitary history, hypotension, weakness, vomiting, abdominal pain, hyponatraemia, hypoglycaemia and response to resuscitation.
What should a patient do if they vomit their oral steroid during illness?
They should follow their personalised sick-day plan. If a repeat oral dose cannot be retained or severe symptoms develop, use the prescribed emergency hydrocortisone injection if available and trained, then seek urgent medical care. Injection is a bridge to assessment, fluids, monitoring and treatment of the cause; it is not a reason to remain at home.
What must be arranged before discharge after an adrenal crisis?
Confirm a sustainable oral replacement regimen, mineralocorticoid plan when primary disease requires it, written sick-day rules, an emergency steroid card, sufficient medicine and an injection kit with demonstrated competence where indicated. Identify the precipitant, reconcile every steroid preparation, provide emergency contact instructions and arrange early endocrine follow-up. Use teach-back rather than documenting education without testing understanding.
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