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 Table of Contents  
EVIDENCE BASED MEDICINE - CASE SCENARIOS
Year : 2018  |  Volume : 16  |  Issue : 2  |  Page : 69-74

Hypocortisolemic crisis: Case scenarios


Department of Endocrinology, Diabetes and Metabolism, Christian Medical College, Vellore, Tamil Nadu, India

Date of Web Publication20-Jun-2018

Correspondence Address:
Dr. H S Asha
Department of Endocrinology, Diabetes and Metabolism, Christian Medical College, Vellore - 632 004, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cmi.cmi_19_18

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How to cite this article:
Asha H S. Hypocortisolemic crisis: Case scenarios. Curr Med Issues 2018;16:69-74

How to cite this URL:
Asha H S. Hypocortisolemic crisis: Case scenarios. Curr Med Issues [serial online] 2018 [cited 2019 Dec 13];16:69-74. Available from: http://www.cmijournal.org/text.asp?2018/16/2/69/234831


  Introduction Top


Hypocortisolemic crisis is a medical emergency which presents with symptoms similar to other conditions such as electrolyte imbalance, hypoglycemia, and hemodynamic shock. This is a potentially life-threatening complication in patients with cortisol deficiency either due to primary adrenal failure, pituitary disease causing secondary adrenal insufficiency, or long-time glucocorticoid use that causes suppression of the hypothalamo–pituitary–adrenal (HPA) axis. Unless the treating physician is aware of the possibility of hypocortisolemia, the diagnosis may be missed. A good history and examination supported by biochemical investigations will guide us to the right diagnosis. The following case scenarios illustrate the clinical complexities involved in diagnosis and management of this problem.


  Case Scenario 1 Top


A 54-year-old female was brought to the emergency department with a history of vomiting and loose stools for 3 days. She was in altered sensorium for the last 1 h. There was no history of head injury. On examination, her Glasgow Coma Scale (GCS) was 9/15; she had tachycardia and hypotension. Her oxygen saturation was normal. She was noted to have striae over the abdomen. Her systemic examination was normal. There were no features of meningitis and there were no focal neurological deficits to suggest cerebrovascular accident.

GRBS was checked because she was in altered sensorium and it was 48 mg/dl. ABG showed PH – 7.36, PO2– 80 mmHg, PCO2 – 35 mmHg, sodium – 126 mmol/L, and potassium – 3.8 mmol/L. Electrocardiography showed sinus tachycardia. In view of hypoglycemia, she was given 100 ml 25% dextrose, followed by isotonic dextrose normal saline. However, her sensorium and hypotension did not improve after the hypoglycemia was corrected.

Questions

  1. What are the possible differential diagnoses you will consider in this case?
  2. Are there any specific clinical clues that would guide you to a diagnosis?
  3. What are the additional laboratory investigations that would help you to diagnose the problem?



  Case Scenario 2 Top


A 30-year-old male was diagnosed to have primary adrenal insufficiency due to adrenal tuberculosis. He was treated with antitubercular therapy (ATT) + prednisolone + fludrocortisone. While on ATT, he was on a higher physiological dose of prednisolone 7.5 mg OD. After completing 9 months course of ATT, he was advised tablet prednisolone 5 mg OD and tablet fludrocortisone 100 mcg OD.

Computed tomography (CT) image of his abdomen [Figure 1] showed bilateral adrenal masses due to tuberculosis – with areas of necrosis and calcification.
Figure 1: Bilateral adrenal masses due to tuberculosis.

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He developed cough with yellowish sputum and fever. Chest X-ray showed right lower zone pneumonia. He was prescribed oral antibiotics for 5 days. Three days after taking antibiotics, though his fever was coming down, he developed 5–6 bouts of vomiting and subsequently complained of being very tired. He was immediately taken to the emergency department. By that time, he was drowsy, but responding to commands. He was hypotensive and hypoglycemic (blood pressure [BP] – 80/50 mmHg, GRBS – 60 mg/dl, and SpO2– 94% on room air). He was diagnosed to have hypocortisolemic crisis. His blood samples were taken for complete blood counts, C-reactive protein (CRP), serum creatinine, and electrolytes. Intravenous (IV) hydrocortisone 100 mg stat followed by 50 mg Q6H was administered. IV 25% dextrose 100 ml stat, followed by DNS 200 ml/h was administered because he was hypoglycemic and hypotensive. IV amoxicillin + clavulanate 1 g q8 h was also started. Subsequently, his sensorium, BP, and other parameters improved (GRBS after 15 min was 100 mg/dl; BP increased to 120/80 mmHg by 1 h; serum sodium – 124 mmol/L; potassium – 5 mmol/L, creatinine – 0.9 mg/dl, and CRP – 56 mg/dl). He was discharged after 2 days.

Subsequently, he was given oral prednisolone 5 mg twice daily for 3 days followed by 5 mg once daily.

Questions

  1. What went wrong that led to hospitalization?
  2. Could this have been prevented?



  Case Scenario 3 Top


A 56-year-old male presented to emergency with sudden onset of severe headache and vomiting (5–6 bouts/day) for 2 days. He had complete ptosis of his left eye for 2 days. On examination, he was conscious and oriented to time, place, and person (GCS-1 5/15). His pulse rate was 96/min; BP was low – 90/60 mmHg. He had complete ptosis of the left eye, frozen left eyeball with no movements of the left eye, and left pupil was dilated with left optic atrophy. He had right temporal hemianopia on visual field testing by confrontation. He had no other neurological deficits. He had decreased facial and body hair. His pubic hair was Tanner's stage 4 and he had 15 ml soft testes bilaterally.

Questions

  1. What is the clinical diagnosis?
  2. What are the investigations and treatment of this problem?



  Discussion of Cases Top


Case scenario 1

Discussion

If the altered sensorium were due to hypoglycemia alone, we would have expected her to recover after the dextrose infusion. There was mild hyponatremia, but this could not explain her poor sensorium.

Blood samples were taken to check serum creatinine, electrolytes, complete blood counts, blood glucose, serum cortisol, and liver function test. Chest X-ray was normal. She was shifted to the Intensive Care Unit (ICU) in view of persistent hypoglycemia with altered sensorium and hypotension, with a suspicion of sepsis.

The ICU registrar observed that she had a rounded face and supraclavicular fullness. She had wide striae over the abdomen; her limbs were thinner in comparison to the rest of her body. Hence, are we dealing with Cushing's syndrome? However, she was hypotensive. The WBC counts and other blood parameters tested were normal.

The two possibilities considered in this scenario were –

  1. Endogenous Cushing's syndrome with septic shock
  2. Hypocortisolemic crisis in an iatrogenic Cushing's syndrome.


Hypocortisolemic crisis was thought to be the most likely problem as the other investigations did not indicate sepsis, and hence she was given 100 mg of IV hydrocortisone. The patient's sensorium recovered and BP improved to 100/70 mmHg in about 30 min. On inquiry, she reported having taken betamethasone 1 mg tablets twice daily for 10 years for bronchial asthma. Investigation reports showed serum sodium of 126 mmol/L, potassium 3.7 mmol/L, and serum cortisol was 1 mcg/dl (normal range 5–15 mcg/dl, >25 mcg/dl during hypotension). The low serum cortisol during the hypotensive state confirmed the diagnosis of hypocortisolemic crisis.

This patient had presented with the classical symptoms of hypoglycemia, hypotension, and hyponatremia suggestive of hypocortisolemic crisis, and in addition, she had a Cushingoid appearance. The reason for the hypocortisolemic crisis was long-term use of potent glucocorticoid at greater than physiological dose which had suppressed her HPA axis. She would have either missed her dose of steroid because of vomiting or she would not have absorbed it, and that had resulted in hypocortisolemic crisis. Steroid misuse can lead to hypocortisolemic crisis during intercurrent illness.

Subsequently, her condition improved and in 1 to 2 days vomiting and loose stools subsided. On discharge, she was advised to take tablet prednisolone 7.5 mg OD (between 7 and 8 am) for 2 months; followed by 5 mg OD (7–8 am) for 2 months; followed by 5 mg (7–8 am) on alternate days for 2 months. She was advised to stop betamethasone. Follow-up was advised after 6 months to assess for recovery of the hypothalamus–pituitary–adrenal axis. In case she experienced hypocortisolemic symptoms such as fatigue, nausea, or vomiting on reducing the dose of prednisolone, she was advised to get back to the previous dose and come for follow-up earlier.

She was also educated about the hydrocortisone stress protocol [Figure 2]. In this situation, she had ended up with hypocortisolemic crisis because she did not get adequate dose of glucocorticoid during her current illness. She was advised that in case of minor illness such as fever, cough, and lower UTI, she should double the dose of tablet prednisolone for 2–3 days until the illness subsides and in case of severe illness or vomiting she should receive injection hydrocortisone IV/intramuscular (IM)-100 mg followed by 50 mg 6 hourly until the illness subsides. The patient and a relative were taught about self-administration of hydrocortisone in case of emergency, especially when medical services are not immediately available such as during midnight, while traveling by bus, train, etc.,
Figure 2: Steroid alert card with hydrocortisone stress protocol.

Click here to view


Patients on long-term steroids should carry a steroid alert card [Figure 2] with them at all times. The card is useful to recognize that the patient is on long-term steroids when they come up with an illness, so that they can be administered hydrocortisone. They are also advised to carry two vials of hydrocortisone and the necessary syringe and sterile water for reconstitution for use in emergency.

In this clinical scenario, the problem which precipitated the crisis was the use of long-term steroids for bronchial asthma. Until we address the primary pathology, her problem will not be adequately resolved, and she may resort to use potent glucocorticoids again for asthma. Hence, she was advised to undergo spirometry after a week and that showed moderate obstructive pattern with significant reversibility suggestive of bronchial asthma. She was started on MDI salmeterol 50 mcg + fluticasone 250 mcg – 2 puffs bipolar disorder and with that her symptoms improved.

The learning points from this case are

  1. Inappropriate long-term use of potent glucocorticoids either in the form of prescribed steroid for a medical condition or occult prescriptions (indigenous medications) are common causes of hypocortisolemic crisis
  2. The treating physician must be aware that some patients may be on unknown prescriptions (ayurvedic or native medicines) which might include steroids, especially if one comes across patients with features of classical Cushing's syndrome and hypocortisolemic crisis. This is especially relevant in individuals with asthma or arthritis. In these situations, one should suspect steroid abuse and treat it appropriately
  3. Hypocortisolemic crisis has a high mortality risk if not recognized and treated quickly. If no facility is available to test for serum cortisol, draw a blood sample for future testing and treat immediately with hydrocortisone
  4. Individuals who have been on more than the physiological dose or on potent steroids for more than 3 weeks will have suppression of the HPA axis. It takes at least 4–6 weeks for recovery of the HPA axis and hence slow tapering of steroids is recommended. In patients who have received steroids for 1–2 years or longer, the tapering would have to be very gradual over a period of 3–6 months, sometimes up to 12–18 months. Some patients may not recover their HPA axis and require long-term physiological steroid replacement.


Hypocortisolemic crisis (adrenal crisis)

This is a potentially life-threatening complication in patients with cortisol deficiency either due to primary adrenal failure, pituitary disease causing secondary adrenal insufficiency, or long time glucocorticoid use that causes suppression of the HPA axis.

Adrenal crisis is defined as worsening of the general condition with signs and symptoms of glucocorticoid and/or mineralocorticoid deficiency along with two of the following conditions: (1)

  1. Nausea or vomiting
  2. Severe fatigue
  3. Hypotension (systolic BP <100 mmHg)
  4. Documented hyponatremia, hyperkalemia, or hypoglycemia.


These features usually resolve after administration of glucocorticoids. The incidence of adrenal crisis is about 6–10 adrenal crises/100 patient-years. The incidence is similar to the incidence of DKA in children which is about 8/100 patient-years. What is most striking here is the fact that a proportion of them die because of unrecognized symptoms or misdiagnosis. The risk of mortality from adrenal crisis is about 0.5/100 patient-years.[1],[2],[3],[4],[5],[6]

How should we taper steroids in patients on long-term steroids, who no longer need them for treatment of the disease condition?

The time duration required for tapering depends on the dose, potency, and duration of the preceding steroid treatment. If the dose of steroid used in the past is known, then change over to an equivalent dose of prednisolone/hydrocortisone, then reduce prednisolone by 5 mg/week up to 20 mg/day, and subsequently, even slower tapering by 2.5 mg every 2 weeks up to 7.5 mg/day of prednisolone.

Subsequently, if you are using prednisolone, taper further by 2.5 mg every 4 weeks and assess HPA axis after 3 months. If you are giving hydrocortisone, then it should be given in three divided doses and taper every 2–3 weeks. If the patient has used a potent steroid for more than 4 years, sometimes it may take about a year for them to recover, and in some situations, it may not be possible to completely withdraw the replacement dose of steroid [Table 1].
Table 1: Steroid tapering schedule from physiological replacement dose

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Assessment of hypothalamo-–pituitary–adrenal axis recovery

It is recommended to do 8 am serum cortisol to assess for HPA axis recovery. If serum cortisol is less than 4 mcg/dl, it is indicative of persistent steroid deficiency and the individual will need glucocorticoid tapering over some more weeks. If serum cortisol (8 am) is between 4 and 15 mcg/dl, you would need an ACTH stimulation test to check whether the axis has recovered. If 8 am serum cortisol is ≥16 mcg/dl, it indicates an adequate cortisol response and you can safely stop the steroid replacement.

The ACTH stimulation tests could be done in two ways.

Short Synacthen test

Synacthen 250 mcg is administered as an IV injection, followed by serum cortisol measurement after 1 h. If post-Synacthen serum cortisol is >18 mcg/dl, it indicates good response implying HPA axis recovery.[7]

Acton Prolongatum test

Synacthen is sparsely available, and hence, we can use Acton Prolongatum which is synthetic corticotrophin carboxymethylcellulose in saline of porcine sequence. Twenty-five units of Acton Prolongatum (60 units/ml) is administered as an IM injection (16 units in a 40 IU insulin syringe) as an alternative. After 1 h, if serum cortisol is >18 mcg/dl, it confirms recovery of HPA axis.[8]

In addition, identify the reason for steroid use and treat it optimally to avoid recurrent steroid abuse.

Case scenario 2

Discussion

Although he was relatively well early in his illness, he required hospital admission after 3 days. During an intercurrent illness, the dose of prednisolone had to be doubled when he developed symptoms of fever and cough. Once he started vomiting more than three bouts, he should have been given IV hydrocortisone, which was also missed. Hence, he ended up in hospital in hypotension.

Learning points

During a minor illness, double the dose of oral steroid in a patient on long-term glucocorticoids.

During severe illness or persistent vomiting follow the stress hydrocortisone protocol and continue IV hydrocortisone until the illness subsides. All patients on long-term steroid therapy should carry with them two vials of injection hydrocortisone, along with sterile water for reconstitution and disposable syringes for emergency injections.

Patients should always carry their steroid alert card and the patient and family should be aware of emergency hydrocortisone injection.

Case scenario 3

Discussion

This is a case of pituitary apoplexy. Clinically, he could either have a nonfunctioning pituitary macroadenoma or macroprolactinoma due to his visual field defects and features of hypogonadism in the form of decreased facial and body hair and soft testes.

His blood investigations showed low serum sodium level of 122; potassium was normal (3.7 mmol/L). Serum potassium increases and sodium decreases in primary adrenal insufficiency due to aldosterone deficiency. Whereas in secondary adrenal insufficiency, potassium is not affected and only hyponatremia occurs due to increased antidiuretic hormone secretion. The serum cortisol was low (1.2 mcg/dl), as expected. Thyroid functions were normal (serum thyroid-stimulating hormone – 2.3uIU/ml, T4 – 10.8 mcg/dl, and free T4 –1.02 ng/dl). Serum testosterone was low (30 ng/dl, luteinizing hormone – 3.4 IU/L, follicle-stimulating hormone – 2.3 IU/L) and prolactin was mildly elevated (59 ng/ml) indicating pituitary stalk compression due to a nonfunctioning pituitary macroadenoma.

Magnetic resonance imaging (MRI) pituitary gland (T1- and T2-weighted images) showed acute hemorrhage into the tumor [Figure 3]a and [Figure 3]b. Postgadolinium contrast MRI [Figure 4] shows hemorrhage into the tumor as a bright spot on top, rest of the pituitary tumor does not take up contrast due to tumor infarction. Only a rim of contrast enhancement is seen consistent with pituitary apoplexy.
Figure 3: (a): Magnetic resonance imaging pituitary gland T1-weighted image. (b) Magnetic resonance imaging pituitary gland T2-weighted image.

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Figure 4: Postgadolinium contrast magnetic resonance imaging pituitary gland showing hemorrhage into the tumor.

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Treatment

The patient was treated with injection hydrocortisone 100 mg IV stat, followed by 50 mg IV Q6H for 48 h; subsequently 25 mg Q6H for 24 h; and then 25 mg IV Q12H for 24 h. Subsequently, tablet prednisolone 5 mg-0-2.5 mg was given from day 3 to 1 week, followed by 5 mg once daily. At discharge, he was also started on injection testosterone (injection testoviron depot 250 mg IM once in 3 weeks) for hypogonadism after confirming the absence of lower urinary tract symptoms and normal PSA. He was advised to come for follow-up with MRI pituitary after 3 months to assess tumor regression following apoplexy.

Learning points

Suspect pituitary apoplexy when you have a patient presenting with sudden onset of severe headache, vomiting, and cranial nerve palsy. The other differentials, in this case, are posterior communicating artery aneurysm or bleed in an intracranial space-occupying lesion.

Hypotension and hypoglycemia are clues to hypocortisolemic crisis. Immediately send blood samples for electrolytes, creatinine, and cortisol. Start injection hydrocortisone without waiting for the results.

Most pituitary tumors spontaneously shrink when they undergo apoplexy because of infarction of the tumor. As a result, most patients with a pituitary apoplexy will not need an emergency surgery unless there is worsening of visual field defect. Repeat imaging of the pituitary has to be done after 3 months to check if there is any remaining viable tumor that requires surgical excision.

In this case, we saw that though the entire pituitary seemed infarcted and there was acute hemorrhage, the thyroid functions were normal initially. This is because T4 has a long half-life of 7 days and hence central hypothyroidism will be evident only after 4 weeks. Hence, repeat thyroid function tests after 1–2 months.


  Could We Have Prevented These Hypocortisolemic Crises? Top


Case 1

Yes, we could have prevented it. If we knew that the patient was on long-term steroids, the asthma could have been treated better, she would have been advised a slow tapering schedule of steroids to facilitate recovery of her HPA axis and she would have been advised on stress hydrocortisone protocol.

Case 2

In case 2, it was already known that the patient had primary adrenal insufficiency. During the intercurrent illness, steroid dose could have been doubled and we could have prevented the hypocortisolemic crisis.

Case 3

In case 3, the patient presented as an acute emergency. The patient himself was not aware that he had a pituitary tumor. Hence, we could not have prevented the hypocortisolemic crisis.


  Precipitating Factors for Adrenal Crisis Top


The most common cause of adrenal crisis in both primary and secondary adrenal insufficiency is gastrointestinal upset, that is, either diarrhea or vomiting, as we saw in our patients, and infections are the second common cause. The less common causes are missing medications, inadequate medications, or psychological stress [Table 2].[9]
Table 2: Causes of adrenal crisis

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The Endocrine Society guidelines [1] recommend that all patients on glucocorticoids should be educated about steroid management during illness, which includes doubling the dose of glucocorticoids during minor illness, fever or stress, and about self-administration of hydrocortisone injection during severe illness or vomiting. All patients should carry a steroid emergency card or medical alert identification to inform health personnel of the need for increased glucocorticoid doses to avert or treat adrenal crisis.

A postal survey of 178 patients with adrenal insufficiency was done in UK in 2006, where they used a questionnaire to assess how patients would respond during an adrenal crisis. It was found that only two-thirds (68%) of patients had an in-date supply of injectable hydrocortisone to treat themselves during emergency, and only 12% were able to self inject hydrocortisone. In 17% of cases, it was administered by a partner, relative, friend, or neighbor. However, over two-thirds of patients relied on medical care facility to get their first dose of hydrocortisone injection in an emergency situation (4% by ambulance personnel, 23% by general practice/nurse, and 38% by other hospital personnel). Obviously, there is a definite need to improve on patient education.[5]


  Glucocorticoid Education and Adrenal Crisis Top


Another study from Germany assessed whether detailed instructions to patients would help them manage their adrenal crisis better. Detailed verbal as well as written instructions were given to 423 patients with adrenal insufficiency (primary adrenal insufficiency – 221; secondary adrenal insufficiency – 202). They were assessed periodically at 6-month intervals with follow-up questionnaires and were prospectively followed up for 2 years. Among 363 patients who completed this study, there were 8.3 adrenal crises/100 patient-years. Those who already had adrenal crisis were at higher risk of recurrent adrenal crisis. Despite patient education, there were about 0.5 adrenal crisis-related deaths/100 patient-years.[10] From this study, it is evident that it is not adequate to educate these patients at one point; the importance of recognition and management of hypocortisolemic crisis should be emphasized during each clinical visit.


  Summary Top


  • Exogenous steroid abuse is a common suspect when a patient has Cushingoid features and presents with hypocortisolemic crisis
  • Increase the dose of steroid replacement during minor intercurrent illness to avoid adrenal crisis
  • In pituitary apoplexy (with the classical triad of headache, vomiting, and cranial nerve palsy), hypocortisolemic crisis should be suspected, and the patient must be treated immediately without waiting for serum cortisol report
  • Steroid education is essential for all patients on long-term steroid therapy. Recognition and management of hypocortisolemic crisis should be emphasized at each clinic visit
  • Steroid alert card is useful for early identification and treatment.


Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Bornstein SR, Allolio B, Arlt W, Barthel A, Don-Wauchope A, Hammer GD, et al. Diagnosis and treatment of primary adrenal insufficiency: An endocrine society clinical practice guideline. J Clin Endocrinol Metab 2016;101:364-89.  Back to cited text no. 1
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2.
Rewers A, Chase HP, Mackenzie T, Walravens P, Roback M, Rewers M, et al. Predictors of acute complications in children with type 1 diabetes. JAMA 2002;287:2511-8.  Back to cited text no. 2
[PUBMED]    
3.
Hahner S, Loeffler M, Bleicken B, Drechsler C, Milovanovic D, Fassnacht M, et al. Epidemiology of adrenal crisis in chronic adrenal insufficiency: The need for new prevention strategies. Eur J Endocrinol 2010;162:597-602.  Back to cited text no. 3
[PUBMED]    
4.
Realsen J, Goettle H, Chase HP. Morbidity and mortality of diabetic ketoacidosis with and without insulin pump care. Diabetes Technol Ther 2012;14:1149-54.  Back to cited text no. 4
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5.
White K, Arlt W. Adrenal crisis in treated Addison's disease: A predictable but under-managed event. Eur J Endocrinol 2010;162:115-20.  Back to cited text no. 5
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6.
Hahner S, Spinnler C, Fassnacht M, Stritt SB, Lang K, Milovanovic D, et al. High incidence of adrenal crisis in educated patients with chronic adrenal insufficiency: A prospective study. Clin Endocrinol Metab 2015;100:407-16.  Back to cited text no. 6
    
7.
Kane KF, Emery P, Sheppard MC, Stewart PM. Assessing the hypothalamo-pituitary-adrenal axis in patients on long-term glucocorticoid therapy: The short synacthen versus the insulin tolerance test. QJM 1995;88:263-7.  Back to cited text no. 7
[PUBMED]    
8.
Gundgurthi A, Garg MK, Dutta MK, Pakhetra R. Intramuscular ACTH stimulation test for assessment of adrenal function. J Assoc Physicians India 2013;61:320-4.  Back to cited text no. 8
[PUBMED]    
9.
Puar TH, Stikkelbroeck NM, Smans LC, Zelissen PM, Hermus AR. Adrenal crisis: Still a deadly event in the 21st century. Am J Med 2016;129:339.e1-9.  Back to cited text no. 9
    
10.
Hahner S, Spinnler C, Fassnacht M, Burger-Stritt S, Lang K, Milovanovic D, et al. High incidence of adrenal crisis in educated patients with chronic adrenal insufficiency: A prospective study. J Clin Endocrinol Metab 2015;100:407-16.  Back to cited text no. 10
[PUBMED]    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2]



 

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  In this article
Introduction
Case Scenario 1
Case Scenario 2
Case Scenario 3
Discussion of Cases
Could We Have Pr...
Precipitating Fa...
Glucocorticoid E...
Summary
References
Article Figures
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