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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Adrenal crisis

Endocrinology and metabolism · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Time-critical presentation

Adrenal crisis is immediately life-threatening. Give hydrocortisone 100 mg IV or IM at once, begin rapid 0.9% sodium chloride resuscitation with haemodynamic reassessment, treat hypoglycaemia and call senior acute, endocrine and critical-care help; diagnostic testing must never postpone therapy.

Overview

Identify adrenal crisis clinically, deliver hydrocortisone and fluid resuscitation without delay, correct complications and convert recovery into a robust prevention plan.

Adrenal crisis is acute cortisol deficiency with physiological decompensation. Reduced vascular responsiveness and intravascular depletion cause hypotension; impaired gluconeogenesis contributes to hypoglycaemia; cortisol deficiency increases vasopressin and worsens hyponatraemia. Primary disease may add aldosterone loss and hyperkalaemia, but central or steroid-induced crises may not.

Diagnosis is clinical at the treatment point. A patient with known adrenal insufficiency may present after vomiting prevents oral absorption, while previously unrecognised disease can first appear during infection. Exogenous steroids across several routes can suppress the axis, so absence of an Addison's label or classic pigmentation is not reassuring.

Emergency treatment is deliberately simple and high consequence: hydrocortisone, isotonic fluid, glucose when needed, monitoring and precipitant control. Detailed localisation and dynamic testing belong after stabilisation. Pregnancy does not justify withholding hydrocortisone; maternal under-treatment endangers both mother and fetus.

Key points

  • Think of crisis in unexplained hypotension or shock, especially with vomiting, abdominal pain, fever, confusion, hypoglycaemia, hyponatraemia, hyperkalaemia or a steroid history.

Aetiology

01

Established adrenal insufficiency

Infection, trauma, surgery or labour can exceed usual cortisol replacement, while vomiting or diarrhoea prevents oral absorption and accelerates volume loss.

02

Glucocorticoid suppression

Recent reduction, abrupt cessation or interacting use of exogenous glucocorticoids can leave the hypothalamic-pituitary-adrenal axis unable to mount an adequate stress response.

03

Previously unrecognised adrenal disease

Primary adrenal or pituitary disease may first become apparent during intercurrent illness, even without pigmentation, hyperkalaemia or a known Addison's diagnosis.

Pathophysiology

  1. 1
    Cortisol availability falls

    Acute cortisol deficiency reduces vascular responsiveness to catecholamines and limits the metabolic response required during infection, injury or another major physiological stress.

  2. 2
    Circulating volume contracts

    Vomiting, diarrhoea and mineralocorticoid loss in primary disease deplete intravascular volume, compounding vasodilatation and producing hypotension or shock.

  3. 3
    Metabolic instability develops

    Impaired gluconeogenesis contributes to hypoglycaemia, while increased vasopressin impairs free-water excretion and worsens hyponatraemia; primary disease may also cause hyperkalaemia.

Clinical features and red flags

Circulatory failureRed flag

Postural or persistent hypotension, tachycardia, cool peripheries, prolonged capillary refill, oliguria or shock may be prominent. Relative bradycardia does not exclude crisis when medicines or conduction disease are present.

Gastrointestinal presentationRed flag

Nausea, repeated vomiting, diarrhoea and severe abdominal pain can mimic a surgical abdomen or gastroenteritis. They also prevent oral steroid absorption and accelerate volume loss.

Neurometabolic changeRed flag

Profound weakness, drowsiness, delirium, seizure or coma may reflect hypotension, hyponatraemia or hypoglycaemia. Check bedside glucose immediately while resuscitation begins.

High-risk historyRed flag

Known adrenal failure, pituitary disease, recent glucocorticoid reduction, multiple steroid routes, immunotherapy, bilateral adrenal disease or a Steroid Emergency Card materially raises pre-test probability.

Laboratory patternRed flag

Hyponatraemia, hyperkalaemia, raised urea/creatinine, low glucose, eosinophilia or hypercalcaemia can support the diagnosis, yet none is sufficiently sensitive to delay or withhold empirical treatment.

Investigations

  1. 01
    ABCDE observations and bedside glucoseFirst step
    Why
    Quantify immediate physiological threat and treat reversible hypoglycaemia.
    Interpretation and limitations
    Record mental state, temperature, oxygenation, heart rate, blood pressure including trend and perfusion. A low glucose needs prompt IV glucose according to the local emergency protocol.
  2. 02
    Cortisol and ACTH before steroid if no delay
    Why
    Preserve evidence for later diagnosis and localisation in a previously undiagnosed patient.
    Interpretation and limitations
    Draw and label exact time before hydrocortisone only when immediately feasible. Acute illness should increase cortisol, so an inappropriately low value is concerning; endocrinology interprets assay and ACTH handling.
  3. 03
    U&E, glucose, FBC, CRP, renal and liver profile
    Why
    Measure electrolyte, renal and inflammatory consequences and search for a trigger.
    Interpretation and limitations
    Trend sodium during rehydration to avoid overly rapid correction. Potassium may be raised in primary disease, while infection can be present without a dramatic inflammatory response.
  4. 04
    Blood cultures, urine studies and targeted microbiology
    Why
    Identify infection without delaying antibiotics in sepsis.
    Interpretation and limitations
    Select tests from source assessment and local sepsis guidance. Fever may arise from infection or crisis stress, so use clinical evidence rather than one marker.

Differential diagnosis

01

Septic shock

Fever, vasodilatation and organ dysfunction may look identical; infection can also precipitate adrenal crisis, so antimicrobial assessment and cortisol protection often proceed together.

02

Gastroenteritis or surgical abdomen

Vomiting, diarrhoea and severe abdominal pain can dominate both presentations, but steroid dependence, hypotension, hypoglycaemia or electrolyte disturbance raises concern for cortisol deficiency.

03

Cardiogenic or obstructive shock

Chest findings, raised venous pressure, focal cardiac signs or persistent shock despite fluid and glucocorticoid treatment should prompt urgent reassessment for another circulatory cause.

Management

01First ten minutesTreat on suspicionFirst stepCompatible acute illness with hypotension, vomiting, altered consciousness or major adrenal risk.+
  1. 1Call for senior help, start ABCDE monitoring, establish IV access and check bedside glucose; draw cortisol/ACTH and routine bloods only if instantly available.
  2. 2Give hydrocortisone 100 mg IV or IM immediately and begin rapid 0.9% sodium chloride, repeatedly reassessing perfusion, lungs, urine output and comorbidity.
  3. 3Correct hypoglycaemia, severe hyperkalaemia and other life threats using local emergency protocols; start sepsis treatment promptly when infection is suspected.
02First daySustain cortisol and find the triggerAfter the initial hydrocortisone bolus and fluid resuscitation have begun.+
  1. 1Continue hydrocortisone 200 mg per 24 hours by infusion or 50 mg IV/IM every six hours, with endocrine and acute-team review.

Complications

01

Refractory shock

Loss of cortisol-mediated vascular tone and progressive volume depletion can produce circulatory collapse, acute kidney injury and critical organ hypoperfusion.

02

Neurological injury

Hypoglycaemia, severe hyponatraemia and hypotension can cause delirium, seizure, coma or secondary cerebral injury if physiological instability persists.

03

Recurrent crisis

Inadequate sick-day education, inaccessible injection supplies or unclear cross-service plans leave the same absorption or stress problem able to trigger another emergency.

Monitoring and follow-up

  • Record blood pressure, heart rate, perfusion, respiratory status and mental state frequently until stable; use critical-care escalation when shock persists.
  • Measure bedside glucose repeatedly after treatment and during reduced intake, with greater vigilance in children, pregnancy, diabetes or sepsis.
  • Trend sodium, potassium, urea and creatinine during fluid and steroid treatment; manage sodium correction rate under the local hyponatraemia policy.
  • Maintain strict input, urine output and cumulative fluid balance, and examine for pulmonary congestion while replacing substantial volume.
  • Audit the prevention bundle before discharge: oral supply, emergency injection, card, education, carer competence, expiry dates and follow-up appointment.

Special situations

A normal potassium can mislead

Crisis from pituitary or exogenous steroid suppression preserves aldosterone. Vomiting and prior fluids can also lower potassium, so the emergency diagnosis is never electrolyte-dependent.

Intramuscular is a feature

When IV access is delayed, the recommended hydrocortisone can be given intramuscularly. Repeated failed cannulation must not become a reason for untreated cortisol deficiency.

Hydrocortisone covers mineralocorticoid temporarily

At crisis doses hydrocortisone supplies substantial mineralocorticoid activity, so fludrocortisone is usually reconsidered as the glucocorticoid dose falls rather than prioritised during shock.

Pregnancy does not lower the dose

Placental metabolism of hydrocortisone protects the fetus, while failure to treat maternal crisis can be catastrophic. Give emergency therapy and involve obstetric medicine urgently.

Every crisis is a systems signal

Missed sick-day escalation, inaccessible injections, vomiting without a backup plan and poor peri-operative communication are modifiable causes. The discharge review should find and close that gap.

Common pitfalls

  1. 01

    Waiting for cortisol, ACTH or a Synacthen result before administering hydrocortisone.

  2. 02

    Withholding treatment because pigmentation, hyperkalaemia or a previous Addison's diagnosis is absent.

  3. 03

    Persisting with oral stress doses despite repeated vomiting and unreliable absorption.

  4. 04

    Giving a large fluid prescription without reassessing lungs, urine output, sodium and cardiac status.

  5. 05

    Assuming continuing hypotension must be adrenal and failing to reassess sepsis, haemorrhage or obstructive shock.

  6. 06

    Discharging after recovery without injection training, spare medication and a written cross-setting plan.

Practice

Two practice questions

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Endocrinology and metabolismOriginal SBA

Immediate crisis treatment

A patient with known primary adrenal insufficiency has vomiting, confusion and blood pressure 78/46 mmHg. What treatment should be given immediately?

Choose one answer, then submit
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Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • Society for Endocrinology adrenal crisis guidanceImmediate hydrocortisone, fluid and ongoing dosing recommendations.
  • NICE NG243 adrenal insufficiency recommendationsNational crisis recognition, emergency treatment and discharge prevention guidance.
  • BNF hydrocortisone monographUK routes, emergency use and steroid-card safety information.
  • Society for Endocrinology exogenous steroid risk documentRisk groups and emergency cover for steroid-induced adrenal suppression.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
The Society for Endocrinology states that suspected crisis should receive hydrocortisone without delay; short-term high-dose glucocorticoid is far safer than missing the diagnosis.
  • Administer 100 mg hydrocortisone intravenously or intramuscularly immediately, then 200 mg over 24 hours by continuous infusion or 50 mg every six hours until clinical recovery and endocrine review.
  • Restore circulating volume using 0.9% sodium chloride, adjusting rate and total to blood pressure, urine output, sodium, heart failure and kidney status rather than giving an unobserved fixed volume.
  • Take paired cortisol and ACTH before hydrocortisone only when tubes and access are ready and sampling creates no treatment delay. Never await the result.
  • Normal potassium does not exclude crisis, particularly in secondary or glucocorticoid-induced insufficiency where aldosterone remains intact.
  • Find and treat the precipitant: gastroenteritis, infection, trauma, surgery, labour, missed or abruptly stopped steroids, failure to stress-dose, poor absorption or an enzyme-inducing interaction.
  • If shock persists after steroid and fluid, reassess ABCDE, sepsis, haemorrhage, cardiogenic or obstructive causes, adequacy of access and critical-care needs rather than attributing everything to cortisol deficiency.
  • Before discharge, convert safely to oral replacement, provide sick-day education and injection competence, replace expired supplies and report a clear written plan to primary and specialist care.
  • 05
    ECG and continuous monitoring
    Why
    Detect hyperkalaemic changes, ischaemia or arrhythmia during shock and electrolyte correction.
    Interpretation and limitations
    Treat life-threatening hyperkalaemia by the emergency protocol in parallel; a normal ECG does not establish a safe potassium concentration.
  • 06
    Focused imaging
    Why
    Investigate precipitating infection, haemorrhage, infarction or another shock cause after initial stabilisation.
    Interpretation and limitations
    CT may reveal bilateral adrenal haemorrhage in an appropriate anticoagulation, sepsis or thrombotic context, but transport must not interrupt resuscitation.
    • 2
    Chart frequent observations, fluid balance, glucose and electrolytes; tailor ongoing isotonic fluid to response and prevent overly rapid sodium correction or pulmonary overload.
  • 3EscalationTreat the precipitant and reconsider the differential if haemodynamics fail to improve, escalating vasopressor and organ support through critical care when required.
    • 03RecoveryMove from rescue to preventionHaemodynamic recovery, improving precipitant and reliable oral intake.+
    1. 1With endocrinology, step down to an appropriate oral stress regimen and then maintenance; restart fludrocortisone in primary disease when high-dose hydrocortisone no longer supplies sufficient mineralocorticoid effect.
    2. 2Establish or confirm diagnosis after recovery with ACTH, renin/aldosterone, dynamic testing and aetiology investigations as appropriate; do not perform them blindly during resuscitation.
    3. 3Before discharge, rehearse sick-day rules and injection technique, issue cards and supplies, document the trigger and send an explicit plan to the GP, pharmacy and endocrine service.
    Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
    Restores essential glucocorticoid activity and vascular responsiveness in suspected adrenal crisis; treatment precedes biochemical confirmation.

    Hydrocortisone emergency injection

    100 mg IV or IM immediately, followed by 200 mg over 24 hours or 50 mg IV or IM every six hours.

    There is no meaningful short-term overdose concern in this emergency. Do not delay for cannulation because IM administration is acceptable, and document exact dose and time.

    Corrects intravascular depletion and sodium loss, improving perfusion alongside hydrocortisone.

    Sodium chloride 0.9% intravenous fluid

    Give rapid initial resuscitation, then individualise further volume and rate from haemodynamics, sodium trend, urine output, renal function and cardiac status.

    Repeatedly assess for pulmonary oedema in older adults, heart failure and renal impairment. Avoid overly rapid correction of chronic severe hyponatraemia and use local fluid guidance.

    Treats a potentially fatal metabolic consequence while cortisol replacement restores glucose regulation.

    Intravenous glucose for hypoglycaemia

    Use the local adult hypoglycaemia concentration and volume with immediate repeat bedside glucose and ongoing substrate once consciousness and swallowing permit.

    Protect the airway, confirm IV patency and prevent recurrent hypoglycaemia with monitoring and appropriate ongoing carbohydrate. Thiamine considerations must not postpone rescue in severe hypoglycaemia.