Adrenal Crisis


Article Author:
Ghada Elshimy
Faysal Alghoula


Article Editor:
Jordan Jeong


Editors In Chief:
Kranthi Sitammagari
Mayank Singhal


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
8/22/2019 3:29:54 PM

Introduction

Adrenal crisis, also termed acute adrenal insufficiency is an acute life-threatening condition with a mortality rate of 0.5/100 patients/year. It is considered one of the endocrine emergency precipitated by an internal or external process in the setting of known or unknown lack of production of the adrenal hormone cortisol, the major glucocorticoid. Early identification and prompt management can save the patient's life and impact survival. The clinicians should be able to differentiate between adrenal insufficiency and adrenal crisis since the adrenal crisis is fatal if left untreated. While this disease is well described, it is often difficult to recognize, and treatment initiation may be delayed leading to notable morbidity and mortality.[1][2][3][4][5][6][7][8]

Etiology

In 1855, Thomas Addison described the first case of adrenal insufficiency. Tuberculosis was the most common cause (70%) during the 1930s. In 1856, Trousseau termed the adrenal insufficiency as “bronze Addison’s disease” which later has become known widely as Addison’s disease. With the discovery of cortisone by Hench, Kendall, and Reichstein in the late 1940s, the life expectancy of patients with adrenal insufficiency dramatically improved and initial data suggested that life expectancy was normalized. There are multiple precipitating factors including:

  1. Infections: bacterial(Streptococcus, Pseudomonas, Hemophilus influenza, Treponema pallidum/Syphilis ( reported in case reports)), mycobacteria, fungal(Histoplasmosis, Pneumocystis Carini, Candida), parasitic (Toxoplasmosis, African trypanosomiasis) or viral(HIV, Herpes Simplex, CMV, Echovirus)
  2. Trauma
  3. Pregnancy
  4. Surgery
  5. Emotional stress
  6. Strenuous physical activity
  7. Thyrotoxicosis( as it increases cortisol metabolism)
  8. Medications: Antiadrenal medications, mitotane, metyrapone, anticancer medications, immune checkpoint inhibitors, tyrosine kinase inhibitors(sunitinib, imatinib), ketoconazole, fluconazole, etomidate, rifampicin, cyproterone acetate, diuretics, and megestrol acetate.
  9. Gastrointestinal (GI) illness, etc
  10. Hot weather
  11. Dehydration ( Diabetes insipidus leads to dehydration and can be a precipitating factor for adrenal crisis)
  12. Alcohol intoxication
  13. Severe migraine 
  14. Seizures
  15. Acute myeloid leukemia (reported in a case report)
  16. Unknown causes

However, regardless of the etiology, the adrenal crisis is an acute complication of adrenal insufficiency. There are several causes of adrenal insufficiency which can be broken down into primary, secondary, tertiary as well as glucocorticoid-induced.  While the most common cause of the adrenal crisis is a sudden withdrawal of long-term corticosteroid therapy (usually more than 5 mg prednisone and greater than 4 weeks), there are many other clinically important and often missed etiologies that can lead to significant mortality.

Primary causes can be simplified to include etiologies that affect the adrenal gland directly, most notably Addison's disease, which can involve the autoimmune destruction of the adrenal gland. Other primary causes can include surgical removal, congenital adrenal disorders, bilateral adrenal hemorrhage, adrenomyeloneuropathy/ adrenoleukodystrophy and infections as tuberculosis, systemic fungal infection, and AIDS. In the setting of meningitis, Waterhouse-Friderichsen Syndrome can precipitate adrenal crises. Adrenal insufficiency is also part of autoimmune polyglandular endocrinopathy type 1,2 and 4 so other endocrine diseases should be ruled out. 

Secondary causes of adrenal insufficiency are due to a disruption of the regulation of cortisol usually from the compromise of the pituitary gland which produces ACTH, which stimulates cortisol release from the adrenal gland. The most common cause is chronic exogenous glucocorticoid use. Other causes include pituitary tumors/metastasis, pituitary apoplexy, pituitary surgery, radiation, lymphocytic hypophysitis, head trauma, Sheehan syndrome in pregnancy, pituitary infiltrative disease, Empty-Sella syndrome, etc.

Tertiary causes refer to disruption of the hypothalamus which in turn affects ACTH release.[9][10][11][12][13][14][5][7][15][16][17]

Epidemiology

The exact frequency of adrenal crisis in the general population is difficult to estimate. The estimated incidence in Europe range from 4.4 to 6.2 new cases/million/year in different studies. The reported prevalence in Europe has been increasing over time. It was initially 39 cases/million in England in 1968 then the number increased to 60 in Denmark in 1974 then 93 in Coventry (UK) in 1992. The number of cases continued to increase to reach 110 cases/million in Nottingham (UK) in 1993 then 117 in Italy in 1996 and lastly 144 in Norway in 2007. The highest prevalence has been reported in Iceland in 2016, with 221 cases/million. Remaining data from all over the world have been sparse. Most of the studies estimated the risk of an adrenal crisis occurring in a patient with adrenal insufficiency to be about 6-10 cases per 100 patient-years (PY). There have been reports of increased risk of adrenal crisis in the elderly (older than 60 years old) with no difference between males and females. Also, there were reports of an increased incidence in patients with thyroid or other endocrine disorders. Patients with autoimmune polyglandular endocrinopathy have a higher incidence to develop adrenal insufficiency (10.9/100 patient/year). In addition, patients with type 1 diabetes, the incidence of adrenal insufficiency increases up to 12.5/100 patients/year.[18][19][20][5][21]

Pathophysiology

The pathophysiology of adrenal crisis formation is not fully understood. It is considered as a mismatch between the need and the use of cortisol. Elevated cortisol level during stress due to the stimulation of the hypothalamic-pituitary axis (HPA) leading to an increase in ACTH which therefore increases the cortisol level. However, some studies showed paradoxically low ACTH in the setting of stress.[22][23]

The adrenal gland's main function is to produce both mineralocorticoids and glucocorticoids. There are other hormones secreted by the adrenal glands including catecholamines and precursors of sex hormones. The adrenocorticotropin hormone (ACTH) is produced by the pituitary gland and its main function is to stimulate the cortisol release from the adrenal glands. Based on the underlying reason for insufficiency (primary vs. secondary) there will be deficiencies in either both mineralocorticoids (aldosterone) and glucocorticoids (cortisol) or simply a deficiency in glucocorticoids alone. The main function of aldosterone is sodium retention and potassium secretion. The cortisol promotes gluconeogenesis, increases sensitivity to catecholamines, and regulates the immune system. If a patient with primary insufficiency has an adrenal crisis, they may be found to be hyponatremic and hyperkalemic in addition to having hypoglycemia and hypotension due to both aldosterone and cortisol deficiency, respectively. Patients with isolated cortisol deficiency may have only hypoglycemia due to impaired gluconeogenesis and hypotension due to decreased sensitivity to catecholamines. This is why hypotension is often refractory to vasopressors. Stressors that precipitate adrenal crisis also release inflammatory cytokines including Tumor necrosis factor (TNF)-alpha, interleukin 1 and 6 which activate HPA. Cortisol works to regulate these cytokines. One cytokine, TNF-alpha, can promote cortisol resistance. In the absence of cortisol in the case of adrenal insufficiency, the TNF-alpha release and sensitivity increase leading to further cortisol resistance which increases the mortality in patients with adrenal crises despite appropriate treatment especially when treatment or recognition is delayed. In healthy subjects, glucocorticoids enhance the synthesis of an enzyme that converts norepinephrine into epinephrine. In the case of adrenal insufficiency, the basal and stress-induced epinephrine release may be impaired and be responsible for hypotension or hypoglycemia during crisis situations. [24][25][26]

Histopathology

The histology of the adrenal gland will depend on the cause of the crisis and the precipitating factor. Usually, there is no histology available unless there is a need for adrenalectomy. The histological characteristics can be variable, including bilateral adrenal hemorrhage, infiltrative disease like sarcoidosis, hemochromatosis, adrenocortical carcinoma, metastasis from kidney carcinoma, lung carcinoma, breast carcinoma, and melanoma or even adrenal lymphomas.[27][5]

History and Physical

Obtaining an extensive history is the initial step in the evaluation in patients with suspected adrenal crisis. A review of the patient's past medical history and past surgical history is mandatory. The physicians should review the list of home medications. Identifying the precipitating factors and confirming if there is any history of long-term steroid use is required as abrupt cessation or an acute process can precipitate adrenal crises in these patients. Inquiring about other autoimmune diseases is also important while obtaining history since a patient with autoimmune polyglandular endocrinopathy can present with multiple autoimmune diseases. Note that recurrent hypoglycemia can be a sign of adrenal insufficiency in patients with type 1 diabetes on insulin therapy. Patients with adrenal crisis usually present with an unexplained shock which is refractory to vasopressors and fluids. Classical manifestations are weakness and fatigue (74–100%) and weight loss (78–100%) with decreased appetite. In children, weight loss with failure to thrive can be seen in 61–100% and other manifestations can be hypoglycemic crises with seizures. Additional manifestations as anorexia, orthostatic hypotension and tachycardia can be seen in 88–94% of the patients while skin and mucosal hyperpigmentation in 80–94%. The gastrointestinal manifestations can be either nausea, vomiting, and diarrhea which occur in 75–86% or recurrent abdominal pain which occur in 31% of the patients. The less common presentation are a surgical emergency, amenorrhea, libido reduction, depression in less than 40% of the patients and the least common presentation is salt-craving which is only seen in 9–16% of the patients. Pregnant patients, patients with meningitis and patients with a headache and vision changes represent a small subset of patients that may present with occult adrenal crisis secondary to Sheehan syndrome, Waterhouse-Friedrichsen syndrome, and pituitary apoplexy respectively. Patients with pituitary apoplexy may present with a headache and bitemporal hemianopsia in addition to signs of adrenal crisis.[7][5][28][29][30]

Evaluation

There are multiple laboratory abnormalities are expected in the setting of adrenal crisis. The Classic laboratory features may reveal:

  • Hyponatremia( due to mineralocorticoid deficiency)
  • Hyperkalemia ( due to mineralocorticoid deficiency)
  • Hypoglycemia( due to decreased gluconeogenesis and glycogenolysis)
  • Low or low normal ACTH level in secondary adrenal insufficiency and high or high normal ACTH level in primary adrenal insufficiency
  • Hypercalcemia(due to increased intestinal absorption and decreased renal excretion of calcium)
  • Prerenal failure with elevated creatinine level
  • Low aldosterone ( due to mineralocorticoid deficiency)
  • High renin is expected in primary adrenal insufficiency as there is an increase in urinary sodium loss and decreases in the blood volume)
  • Normocytic normochromic Anemia, lymphocytosis, and eosinophilia 
  • TSH levels may be increased, usually between 4 and 10 IU/L( due to coexisting hypothyroidism in autoimmune polyglandular endocrinopathy or due to the lack of the inhibitory effect of cortisol on TSH production)

Other lab tests may also help to reveal the underlying cause of the concomitant adrenal crisis. In patients with known adrenal insufficiency, you may be able to use laboratory findings to distinguish between primary and secondary causes. Patients with secondary adrenal insufficiency may only be hypoglycemic due to impaired gluconeogenesis, but there is some variability overall as this is rare. The mineralocorticoid axis is usually intact and it is not expected to see hyponatremia or hypokalemia in the laboratory testing. In patients where the diagnosis of adrenal crisis is not clear, there are confirmatory tests that may be done, but this should not take precedence over empiric treatment in suspected cases. An ACTH stimulation test would confirm the diagnosis but should not be done in the acute setting. Several labs such as ACTH, serum cortisol, aldosterone, dehydroepiandrosterone sulfate, and renin should be drawn before the administration of hydrocortisone for review at a later time. In some cases a random cortisol level before administration may exclude or support the diagnosis of adrenal insufficiency and crisis; however, this should not prevent the administration of glucocorticoids when the picture is not clear. A high cortisol level of >20 mg/dL (550 nmol/L) can exclude the diagnosis, while a low cortisol level of <5 mg/dl in the early morning and in the setting of acute illness support the diagnosis. Other investigation for the underlying precipitating factors like infections, infiltrative disease, metastasis should also be addressed. In addition, given the hyponatremia, other autoimmune diseases should be tested including thyroid function tests. Adrenal imaging studies are usually not required unless suspected bilateral adrenal hemorrhage or cancer or in specific cases. Bilateral hyperdense lesions are characteristic for adrenal hemorrhage.  [1][31][32][7][33][34][15]

Treatment / Management

The definitive treatment of adrenal crisis is the administration of glucocorticoids, specifically hydrocortisone. The dose is 100 mg intravenously or intramuscularly (IV/IM) as an initial bolus followed by 100 to 300 mg daily after that for another 2-3 days either as boluses every 6 hours or as continuous infusion until full recovery. At this dosage, hydrocortisone will also provide sufficient mineralocorticoid coverage as well. While hydrocortisone is the preferred treatment, administration of prednisolone or methylprednisolone, and dexamethasone has been described. In addition to medical therapy, these individuals also require aggressive fluid and vasopressor management. A thorough search should also be made for the cause, and empiric antibiotics are recommended. Close monitoring in the intensive care unit (ICU) is required. Note that if the patient is pregnant, the preferred agent is hydrocortisone and the patient should be discharged on hydrocortisone instead of cortisone acetate. 

Guidelines for managing adrenal crisis during an emergency

  1. If the patient has clinical and laboratory features of adrenal crisis, administer 100 mg hydrocortisone IV every 6-8 hours. 
  2. Since dehydration and hypovolemia are common precipitating factors, rehydration of the patient with normal saline 0.9% is essential ( it will also correct the hypovolemia and the prerenal failure). 1-liter normal saline should be given in the first hour then the need for further intravenous fluid resuscitation should be addressed according to the hemodynamic status of the patient(usually 4–6 liters are needed in the first 24 hours)
  3. Correction of hypoglycemia with intravenous dextrose with frequent monitoring of the blood glucose is essential. 
  4. Avoid rapid correction of hyponatremia ( more than 6-8 meq in the first 24 hours) to avoid osmotic demyelination syndrome (Take into consideration that Cortisol replacement can induce water diuresis and suppress antidiuretic hormone )
  5. The assessment of the urine output is required.
  6. Contact endocrinologist as soon as possible on further advice.
  7. Only taper steroids after there are a clinical improvement and the tapering should be gradual. [35][36][7][37][5][38][39]

Differential Diagnosis

Because the adrenal crisis is rarely an independent process, the differential diagnosis may be very broad depending on the presentation and underlying etiology. While altered mental status, abdominal pain, nausea vomiting, fever, among others are all common presenting symptoms. Hypotension is usually the most significant. In a patient with these symptoms and known adrenal insufficiency, the adrenal crisis should be the top differential. However, there should be further investigation to determine the precipitating cause of the adrenal crisis whether that is sepsis, infection, trauma, physical or emotional stress, myocardial infarction, and so forth. In a patient with no known adrenal pathology who presents with hypotension that is refractory to fluid administration, vasopressor support, and appropriate management otherwise, the diagnosis of adrenal crisis should be considered and adequately ruled out.[5][39]

Prognosis

Adrenal crisis is not a common disease however it has a high mortality. The estimated mortality rate is 0.5/100 patients/year. However, the actual rate of death is difficult to be estimated. There is some data stating that mortality can be as high as 25% of the patients presenting with adrenal crises. Prompt recognition and treatment of both the underlying condition and adrenal crisis may lead to clinical improvement, but in many cases, mortality remains high. However, a Japanese study looking at an adrenal crisis in patients with known insufficiency found a mortality rate of closer to 3% while a German study was just over 6%. In the Japanese study older age, concomitant endocrine disorders and impaired level of consciousness was associated with increased mortality.  Data from the European Adrenal Insufficiency Registry found the major causes of death in patients with AI were cardiovascular disease (35%) and infection (15%). [5][15][3][40][41]

Complications

Even with proper recognition and treatment, the adrenal crisis may result in death. Other complications may include seizures, arrhythmias, coma, etc. due to electrolyte abnormalities such as hyponatremia, hyperkalemia, and hypoglycemia. Hypotension may lead to hypoperfusion and organ failure as well. However, many other complications may arise secondary to the precipitating disease or event.[5][42][3]

Consultations

A critical care evaluation and consultation is needed in these patients as many of them will present with hypotension, altered mental status, and cardiovascular collapse. The severity of their presentations will often necessitate a higher level of care and monitoring which may include vasopressors, fluids, antibiotics and further management depending on the precipitating etiology of the adrenal crisis. Once the diagnosis of adrenal crisis is suspected, an endocrinology consultation should be obtained to confirm the diagnosis or to tailor the proper administration of corticosteroids further as well as to manage any underlying endocrine disorders.

Deterrence and Patient Education

More than 50% of patients with adrenal crisis don't have a prior diagnosis of adrenal insufficiency. Education regarding the diagnosis and the stress dose steroids is a crucial part of the management of an adrenal crisis. The patients should receive the following education:

  • Sick days rule: which includes doubling or tripling the daily oral dose during minor illness.
  • Stress dose is needed during stressful situations including trauma, surgery, major procedures, and severe illness.
  • The patient should be aware of signs and symptoms of adrenal insufficiency including nausea, vomiting, abdominal pain, hypoglycemia, hypotension, weight loss, etc.
  • The importance of wearing medical alert bracelets or necklaces.
  • The patient should have additional supplies at home in case it is needed.
  • An emergency kit should be available in case it is needed(100 mg hydrocortisone sodium succinate for injection or dexamethasone 4 mg, along with vials of sterile 0.9 percent normal saline and syringes )
  • In a special situation like pregnancy, during labor, the patients should receive 25 mg hydrocortisone IV every 6 hours. At the time of the delivery, 100 mg Hydrocortisone should be given. After the delivery, tapering the dose in 3 days is recommended).[5][14][43]

Pearls and Other Issues

An adrenal crisis should be suspected in patients presenting with an acute shock that that is refractory to adequate fluid resuscitation and vasopressors.

Adrenal crisis may be found more often in the elderly and those with other endocrine disorders. Patients with altered mental status and concomitant endocrine disorders may be at risk for higher mortality.

Hyponatremia, hyperkalemia, and/or hypoglycemia may be clues toward a possible diagnosis of adrenal crisis especially in the setting of hypotension.

Hydrocortisone 100 mg IV/IM is the mainstay of treatment and should be given immediately when suspecting an adrenal crisis.

Pregnant patients, patients with meningitis and patients with a headache and vision changes represent a small subset of patients that may present with an occult adrenal crisis.

Enhancing Healthcare Team Outcomes

Given that adrenal crises affect many organs and have a high mortality rate, the disorder is managed by an interprofessional team inside the ICU. This team should include an intensivist, endocrinologist and a radiologist. Other important members of the team include an ICU nurse and a pharmacist. ICU nurses must monitor vitals, urine output, and hemodynamics continuously- and deviation from the standard should be communicated to the interprofessional team. The education of the patients about the disease and its potential complications is of significant importance in the prevention of adrenal crisis. The patient and family should be educated by the nurse and reinforced by the clinician that abrupt cessation of exogenous corticosteroids is the most common cause of the adrenal crisis and this should be avoided. These patients depend heavily on exogenous corticosteroids to maintain their baseline health and they must be extensively educated to monitor for any aberrations and adjust their doses appropriately. Education regarding corticosteroid adverse effects should be performed by both the physician and the pharmacist. Finally, all patients should be encouraged to wear a medical alert bracelet indicating the disorder. [44][45](Level V)

Outcomes

Despite steroids replacement therapy in patients with adrenal crisis, once an adrenal crisis occurs, data show that the majority of patients have a poor quality of life as many patients remain disabled and are no longer able to work given depression and chronic fatigue. In addition, if the cause is due to secondary adrenal insufficiency, this is also associated with an increase in mortality. The cause of the mortality remains unclear, but it is most likely due to respiratory infections, adverse cardiovascular events, and stroke. [1][46](Level V)

 


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Adrenal Crisis - Questions

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A 60-year-old female was found in a semi-comatose condition and brought to the emergency department. On physical exam, her height was 66 inches (167.6 cm), and weight was 123 lb (55.8 kg) (BMI=19.9 kg/m2). Her blood pressure was 80/40 mmHg; her pulse rate was 150 beats/min with temperature 99F. She was disoriented and lethargic with normal deep tendon reflexes. Her home medications include aspirin and ketoconazole prescribed for onychomycosis of her toenails 6 months ago.Laboratory test results demonstrate: hemoglobin 9 g/dl; hematocrit 25%; WBC count 9840 cells/mm3; platelet count 297,000 cells/mm3; creatinine 1.09 mg/dl sodium 128 meq/l; potassium 5.2 mEq/L; chloride 93 mEq/L; and bicarbonate 18 mEq/L. Chest radiography and CT brain didn’t reveal any abnormalities. Blood and urine cultures were sent. The patient was started on intravenous fluid resuscitation with broad-spectrum antibiotics. Which of the following is true regarding this medical condition?



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An elderly diabetic with steroid-dependent asthma undergoes bowel surgery. She is admitted to the intensive care unit in critical condition and requires pressors and mechanical ventilation. On postoperative day three, she develops a fever of 39.2 C, hypotension, and lethargy. Her laboratory values indicate hypoglycemia and hyperkalemia. Which of the following explains her situation?



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A 16-year-old female presented to the emergency department with fever, chills, memory problems and neck rigidity. In the emergency department, she was tachycardiac, hypotensive, and febrile. She had neck stiffness with multiple purple skin rash in the face and the arms. She had a witnessed seizure episode inside the emergency department. Laboratory testing revealed leucocytosis with left shit, hyponatremia, hyperkalemia, and hypercalcemia. Meningitis was suspected and lumbar puncture was performed. She was started on intravenous fluid with broad-spectrum antibiotics . 2 hours afterward, the patient complained of sudden onset severe abdominal pain with persistent vomiting. Which is the following is true regarding the patient medical condition?



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A 16-year-old female presents to the emergency department with confusion, lethargy, and diffuse skin hyperpigmentation. Her sister stated that she has been complaining of gastroenteritis for the past few days. Family history includes type 1 diabetes mellitus in her sister. Her vital signs are temperature 105F, HR: 149/min, BP: 70/40 mmHg, RR: 20/min, and oxygen saturation: 90% on room air. Physical examination is remarkable for significant diffuse skin hyperpigmentation, mild diffuse abdominal tenderness without a rebound. She was confused but able to follow simple commands. Laboratory data demonstrates hyponatremia with hyperkalemia and hypoglycemia. She was given dextrose intravenous and started on intravenous normal saline with broad-spectrum antibiotics; however, the blood pressure remained 70/40 mmHg. Vasopressors were started. What is the most appropriate next step in management?



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A 40-year-old female with a history of HIV and hypertension was brought to the emergency department by her son as she was confused for the past 2 days. She also has been complaining of severe diffuse abdominal pain with nausea and vomiting. Her home medication included megestrol acetate and triumeq (each tablet contains 50 mg dolutegravir, 600 mg abacavir, and 300 mg lamivudine). As per her son, the patient ran out of medication around 2 weeks ago. On physical exam, she was confused. The abdominal exam revealed diffuse tenderness, without rebound tenderness. She had normal deep tendon reflexes. The patient was hypotensive, tachycardiac with hyponatremia, hyperkalemia, and anemia in her laboratory testing. Intravenous fluids were started along with broad-spectrum antibiotics however the patient remained hypotensive requiring vasopressors. Which of the following is true regarding the patient 's medical condition?



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A 60-year-old female presents to the emergency department with altered mental status. She has a history of hypertension, diabetes type 2, Crohn disease, and dyslipidemia. Her home medications are lisinopril 20 mg daily, metformin 1gm Twice daily, atorvastatin 20 mg daily and prednisone 5mg daily. As per her daughter, the patient ran out of medication 1 week ago. In the emergency department, her vital signs are temperature 105F, heart rate: 149/min, blood pressure: 70/40 mmHg, respiratory rate: 20/min, and oxygen saturation: 90% on room air. Physical examination is remarkable for significant diffuse abdominal tenderness. Laboratory data demonstrates hyponatremia, hypercalcemia, normocytic anemia with eosinophilia. Which of the following is correct regarding this medical condition?



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A 60-year-old woman with a history of leukemia was found in a semi-comatose condition and brought to the emergency department. On physical examination, her blood pressure was 80/40 mmHg; her pulse rate was 150 beats/min with temperature 100 F. She was disoriented and lethargic. She was recently started on sunitinib for leukemia treatment. Laboratory test results demonstrate: hemoglobin 9 g/dl; hematocrit 25%; WBC count 9840 cells/mm3; platelet count 297,000 cells/mm3; creatinine 1.09 mg/dl sodium 126 meq/l; potassium 5.2 mEq/L; chloride 93 mEq/L; and bicarbonate 21mEq/L. Chest radiography and CT brain didn’t reveal any abnormalities. Blood and urine cultures were sent. The patient was started on intravenous fluid resuscitation with broad-spectrum antibiotics however hypotension persisted and vasopressors were started. Which of the following is true regarding this medical condition?



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A 28-year-old female with a past medical history of type 1 diabetes was brought to the emergency department as she was complaining of diffuse abdominal pain, fatigue and weight loss for the past 3 weeks. She noticed frequent hypoglycemia episodes in the last 3 weeks despite no changes in her insulin regimen. Her diabetes has been well controlled for many years on an insulin pump and her last hemoglobin A1C was 6.8% 2 months ago. In the emergency department, she had a seizure episode and blood glucose was found to be 28 mg/dl. She was given dextrose and insulin pump was discontinued. The patient has a family history of celiac disease in her sister and multiple sclerosis in her mother. On physical exam, she was confused. The abdominal exam revealed diffuse tenderness, without rebound tenderness. She had normal deep tendon reflexes. There was some hyperpigmentation on her lips and her skin. The patient was hypotensive, tachycardiac, afebrile with hyponatremia and anemia in her laboratory testing. The intravenous fluid was started with broad-spectrum antibiotics however the patient remained hypotensive requiring vasopressors. Which of the following is the least accurate statement regarding the patient 's condition?



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A 17-year-old female is brought to the emergency department by emergency medical services. She is too delirious to give a history but alert enough to complain of stomach pain. She is noted to be hypotensive and tachycardic. She is afebrile. Her exam is unremarkable except for dry mucous membranes. Intravenous fluids are started. Serum chemistry shows that the potassium is elevated and sodium is decreased. Blood glucose is borderline decreased. The electrolytes are otherwise within normal limits. A CBC is unremarkable. After 3 liters of fluids, the patient is still hypotensive. What is the definitive treatment for this patient's condition?



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A patient with Addison disease may experience an acute adrenal crisis. What signs and symptoms listed may appear in a patient in acute adrenal crisis? Select all that apply.



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A patient with rheumatoid arthritis undergoes an emergency appendectomy. Postoperatively, the patient's blood pressure is 86/58 mmHg with a respiratory rate of 6 breaths per minute. What could have been given preoperatively to prevent this presentation?



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Adrenal Crisis - References

References

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