49-year-old male with an adrenal crisis. Appearance, showing lack of facial hair, dehydration, Queen Anne's sign (panel A), pale skin, muscular and weight loss, and loss of body hair (panel B).
The biggest trigger for adrenal crisis is gastrointestinal illness. Those with primary adrenal insufficiency are at a higher risk for an adrenal crisis. The physiological mechanisms underlying an adrenal crisis involve the loss of endogenous glucocorticoids' typical inhibitory effect on inflammatory cytokines.
A tailored prescription, and strategies for administering additional glucocorticoids for physiological stress, are critical preventative measures. When someone experiences an adrenal crisis, they require immediate parenteral hydrocortisone.
About 6–8% of those with adrenal insufficiency experience an adrenal crisis at some point each year. The mortality rate linked to adrenal crises is up to 6%.
Signs and symptoms
In as many as 50% of those with Addison's disease, adrenal crisis can be the first indication of adrenal insufficiency. Diagnosis is often delayed since most of the symptoms of adrenal insufficiency are nonspecific and develop insidiously.[5]Hypotension and shock that fail to respond to vasopressors or fluid resuscitation are the main signs of an adrenal crisis.[6] Those in an adrenal crisis can deteriorate quickly, usually within a few hours.[7]
Exogenous steroid use is the most frequent cause of adrenal insufficiency, and those who use steroids also run the risk of experiencing an adrenal crisis. Adrenal crisis can be triggered by abrupt, and frequently unintentional, steroid withdrawal. The hypothalamic–pituitary–adrenal axis is suppressed by the use of glucocorticoids in rectal, paraspinal, intradermal, intraarticular, injectable, nasal, inhaled, or topical preparations. At pharmacological dosages, medroxyprogesterone and megestrol also exhibit a notable glucocorticoid effect. This risk may increase if steroids are used concurrently with ritonavir which inhibits the liver's CYP3A enzyme that breaks down steroids.[12]
There is a greater risk for adrenal suppression with longer durations, greater doses, and oral and intraarticular preparations of steroids. Nonetheless, no amount, time frame, or mode of administration can reliably predict adrenal insufficiency.[13]
People who have both secondary adrenal insufficiency and diabetes insipidus are more likely to experience an adrenal crisis. This increased risk could be attributed to either the absence of V1-receptor-mediated vasoconstriction in times of stress or the increased risk of dehydration.[15] A higher risk of adrenal crisis has been linked to other medical conditions such as diabetes and asthma, though the exact mechanism is unknown.[16]
Those with adrenal insufficiency have a 50% risk of experiencing an adrenal crisis within their life,[15] and those who have experienced an adrenal crisis in the past are more susceptible to re-developing adrenal crisis.[17]
Triggers
A known precipitating event can be found in over 90% of episodes of adrenal crisis.[5] The most common cause of adrenal crisis is infections, specifically gastrointestinal infections.[14][18] Adrenal crises can also be caused by major surgery, dental operations, pregnancy/labour, extreme weather, serious injury/accidents, intense physical activity, vaccines, and emotional stress.[19]
Cortisol has a 70 to 120-minute half-life meaning that cortisol levels fall within several hours of cortisol deprivation.[21] Because cortisol modulates the transcription of genes containing a glucocorticoid response element, it effects many different genes. The physiological effects of low cortisol begin with the loss of the natural inhibitory function of glucocorticoids on inflammatory cytokines. This leads to sharp rises in cytokine concentrations, which can induce fever, lethargy, anorexia, and pain. As a result, low cortisol causes changes in immune-cell levels, including lymphocytosis, eosinophilia, and neutropenia. Low levels of cortisol means that it loses its ability to work with catecholamines to reduce vascular reactivity, which causes vasodilatation and hypotension. Low cortisol has an adverse effect on the liver's metabolism, resulting in hypoglycemia, decreased gluconeogenesis, lower levels of free fatty acids and amino acids in circulation.[10]
Loss of cortisol suppresses nuclear factor κB (NF-κB) and activator protein 1 (AP-1), which allows genes that generate inflammatory proteins to be activated without restriction. This is because cortisol normally inhibits NF-κB's binding to the glucocorticoid receptor. Additionally, through potassium retention and sodium and water loss, mineralocorticoid deficiency is likely to aggravate adrenal crises.[10]
Diagnosis
Change in plasma cortisol cycle (mcg/dl) over 24 hours
When a person with adrenal insufficiency is known to be exhibiting symptoms of an adrenal crisis, treatment needs to start right away.[15] Diagnostic examinations shouldn't result in a delay in treatment. If adrenal insufficiency is suspected a blood sample should be collected immediately to test serum cortisol and ACTH levels, but treatment should begin while waiting for results. Once an acutely ill person has recovered, the diagnosis can be confirmed.[22]
Adrenal insufficiency can be diagnosed by testing renin, dehydroepiandrosterone sulfate, aldosterone, serum cortisol, and ACTH levels.[15] A high cortisol level of more than 13 to 15 mg/dL can rule out the diagnosis. A low cortisol level of less than 3 mg/dL, obtained in the early morning or during a stressful period, strongly suggests the possibility of adrenal insufficiency.[23] In instances of primary adrenal insufficiency, there is a correspondingly high ACTH level; in contrast, low or inappropriately normal ACTH correlates with tertiary or secondary adrenal insufficiency.[24]
Prevention
A customized prescription as well as a plan for the administration of additional glucocorticoids for physiological stress are important preventative measures. If oral glucocorticoids are not an option, parenteral hydrocortisone should be used, preferably at home. Devices like MedicAlert bracelets and necklaces can alert caregivers to the possibility of adrenal crisis in those who are unable to communicate verbally.[25]
Although the exact dosage has been debated, it is generally agreed upon that anyone with proven adrenal insufficiency should receive glucocorticoid replacement during stressful times.[3] The recommended amounts of glucocorticoid replacement are dependent on the anticipated stress, and the current guidelines depend on expert opinion.[26] Though there may be variations in specific regimens, most agree that stress doses for simple surgery should be quickly tapered and should not last longer than three days. This is because unneeded steroid excess can lead to infections, poor wound healing, and hyperglycemia.[3]
In those who are unable to tolerate oral medication or do not respond to stress doses, a low threshold to initiate parenteral hydrocortisone management should be used to guarantee adequate systemic absorption, since gastroenteritis frequently precedes an adrenal crisis[17] and stress dose glucocorticoids may not always avoid an adrenal crisis.[3]
Those experiencing vomiting, chronic diarrhea, or an imminent adrenal crisis should receive intramuscular hydrocortisone. Individuals must be prepared to administer it themselves because they can rapidly deteriorate.[27] Those with adrenal insufficiency may own a hydrocortisone ampoule,[28] but not all have practiced the injection, and most will depend on medical professionals to give it to them in the event of an adrenal crisis episode. Individuals may experience significant physical as well as cognitive impairment during their illness, which may impair their capacity to make wise decisions or administer medicine.[3] Therefore, everyone with adrenal insufficiency should receive training on intramuscular hydrocortisone use and education on how to recognize an adrenal crisis, as well as assistance from a close family member or friend.[27]
In case an individual suffering from adrenal insufficiency loses consciousness, they must receive the necessary medical attention. Reminding those with adrenal insufficiency to always wear or keep a MedicAlert bracelet or just an emergency card is important. A survey of 46 people with adrenal insufficiency revealed that some medical professionals are reluctant to medicate the condition even when it is brought to their attention, which is a serious cause for concern.[29][30] Only 54% of those with adrenal insufficiency got glucocorticoid administration within 30 minutes of arrival, even though 86% of those with adrenal insufficiency were promptly attended to by a medical professional within forty-five minutes of a distress call.[31]
Treatment
The two foundations of treatment for adrenal crisis are steroid replacement and fluid resuscitation.[3] When adrenal crisis treatment is started as soon as possible, it can be effective in preventing irreversible effects from prolonged hypotension.[32] Treatment should not be postponed while doing diagnostic tests. If there is reason to suspect something, a blood sample could be taken right away for ACTH and serum cortisol testing; however, treatment needs to begin right away, regardless of the results of the assay. Once someone has recovered clinically, it is safe to confirm the diagnosis in an acutely ill person.[22]
In cases of emergency, parenteral hydrocortisone can be given as soon as possible by intramuscular (IM) injection while IV access is being established, or as a bolus injection of 100mg of intravenous (IV) hydrocortisone. After this bolus, 200mg of hydrocortisone should be administered every 24 hours, either continuously by IV infusion or, if that is not possible, in doses of 50mg of hydrocortisone per IV/IM injection every 6 hours.[33]
It is widely acknowledged that extra mineralocorticoid treatment is not necessary at hydrocortisone dosages greater than 50mg/day because there is adequate action within the mineralocorticoid receptor.[3] In those who have primary adrenal insufficiency, fludrocortisone needs to be started with subsequent dose tapering; for most people, a daily dose of 50–200 mcg is adequate.[37]
Those with lymphocytic hypophysitis can experience both adrenal insufficiency as well as diabetes insipidus. Whether or not a someone is receiving treatment for diabetes insipidus, fluid administration should be done carefully because too much fluid can lead to hypernatremia and too little water can cause hyponatremia. Hyponatremia is typically maintained with careful synchronization of urine output and a normal saline infusion.[32]
Outlook
People with hypoadrenalism are more likely to die from adrenal crises; the death rate from adrenal crises can amount to 6% of crisis events.[4] While symptoms may have gone unnoticed prior to the fatal episode, fatal adrenal crises have happened in those who had never been diagnosed with hypoadrenalism.[38]
Epidemiology
An adrenal crisis occurs in roughly 6–8% of those with adrenal insufficiency annually.[39] Those with primary hypoadrenalism experience adrenal crises somewhat more frequently compared to those with secondary adrenal insufficiency. This is likely due to the fact that those with primary hypoadrenalism lack mineralocorticoid secretion and some with secondary adrenal insufficiency retain some cortisol secretion.[16] Despite varying degrees of consequent adrenal suppression, those with hypoadrenalism from long-term glucocorticoid therapy rarely experience adrenal crises.[40]
The treatment of pituitary tumors and the widespread use of opioids for pain, as well as exogenous glucocorticoid therapy for the numerous conditions that become more common in people over 60, are the main causes of a new diagnosis of adrenal insufficiency in older adults.[43][44] Adrenal crisis is more likely to occur in older people.[45]Urinary tract infections, particularly in older women, are often linked to an adrenal crisis, as is pneumonia as well as a flare-up of COPD. Cellulitis is linked to adrenal crises within this age range and may be more prevalent in those with fragile skin who have been exposed to higher doses of glucocorticoids. Older adults frequently experience falls and fractures, which may be linked to postural hypotension, especially in those who have primary adrenal insufficiency.[46]
Older people have a higher mortality rate from adrenal crisis, at least in part due to the existence of comorbidities that make treatment more difficult.[47]
While studies on the prevalence of adrenal crisis in older adults are limited, one population-based study into hospital admissions for adrenal crisis found that the incidence increased with age in older individuals, going from 24.3 (60–69 years) to 35.2 (70–79 years) and 45.8 (80+ years) per million per year. This is significantly higher compared to the general adult admission rate, which is 15.0 per million annually in the same population.[48]
Pregnancy
Most cases of adrenal insufficiency in pregnancy are identified before conception. Because the symptoms of hyperemesis gravidarum (fatigue, vomiting, nausea, and mild hypotension) and normal pregnancy (nausea and vomiting) overlap, there is usually little clinical indication of adrenal insufficiency during pregnancy.[49][50]
Untreated adrenal crisis can cause severe morbidity in both the mother and the fetus, such as inadequate wound healing, infection, venous thromboembolism, extended hospital stays, preterm birth, fetal intrauterine growth restriction, and an increased risk of cesarean delivery. The occurrence of adrenal crisis during pregnancy is uncommon, even in people who have a documented history of adrenal insufficiency. In one study, pregnancy was identified as a trigger for adrenal crisis in 0.2% of the 423 participants. In a different study, only 1.1% of the 93 participants in the study who had a known insufficiency experienced an adrenal crisis during pregnancy.[50]
A common finding in children experiencing an adrenal crisis is hypoglycemia. This can lead to seizures, which can result in permanent brain damage or even death.[51] Due to issues with adrenomedullary development as well as epinephrine production, hypoglycemia may be more prominent in the context of acute adrenal insufficiency in congenital conditions, including congenital adrenal hyperplasia, compared to other forms of primary adrenal insufficiency. The severity of the enzyme impairment is correlated with the degree of adrenomedullary dysfunction.[52] Severe hyperkalemia has also been linked to potentially fatal cardiac arrhythmias.[51]
Studies have demonstrated that younger children with congenital adrenal hyperplasia experience adrenal crisis events more frequently than older children and adolescents.[53] Psychosocial factors can alter the baseline adrenal crisis risk, especially as the transition from parental treatment oversight to self-management in adolescence.[54] Management in this age group is further complicated by changes in cortisol pharmacokinetics, resulting in an increased clearance as well as volume without a change to the cortisol half-life that has been shown during the pubertal period.[55]
There is still a significant morbidity and death associated with adrenal insufficiency in newborns and early children. It has been estimated that 5–10 episodes of adrenal crisis occur for every 100 patient-years in those with adrenal insufficiency; incidences may be higher in specific countries. Adrenal crisis among kids results in death in about 1/200 cases.[56]
The adrenal glands are endocrine glands that produce a variety of hormones including adrenaline and the steroids aldosterone and cortisol. They are found above the kidneys. Each gland has an outer cortex which produces steroid hormones and an inner medulla. The adrenal cortex itself is divided into three main zones: the zona glomerulosa, the zona fasciculata and the zona reticularis.
Cushing's syndrome is a collection of signs and symptoms due to prolonged exposure to glucocorticoids such as cortisol. Signs and symptoms may include high blood pressure, abdominal obesity but with thin arms and legs, reddish stretch marks, a round red face due to facial plethora, a fat lump between the shoulders, weak muscles, weak bones, acne, and fragile skin that heals poorly. Women may have more hair and irregular menstruation. Occasionally there may be changes in mood, headaches, and a chronic feeling of tiredness.
Cortisol is a steroid hormone in the glucocorticoid class of hormones and a stress hormone. When used as medication, it is known as hydrocortisone.
Addison's disease, also known as primary adrenal insufficiency, is a rare long-term endocrine disorder characterized by inadequate production of the steroid hormones cortisol and aldosterone by the two outer layers of the cells of the adrenal glands, causing adrenal insufficiency. Symptoms generally come on slowly and insidiously and may include abdominal pain and gastrointestinal abnormalities, weakness, and weight loss. Darkening of the skin in certain areas may also occur. Under certain circumstances, an adrenal crisis may occur with low blood pressure, vomiting, lower back pain, and loss of consciousness. Mood changes may also occur. Rapid onset of symptoms indicates acute adrenal failure, which is a clinical emergency. An adrenal crisis can be triggered by stress, such as from an injury, surgery, or infection.
Cushing's disease is one cause of Cushing's syndrome characterised by increased secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary. This is most often as a result of a pituitary adenoma or due to excess production of hypothalamus CRH that stimulates the synthesis of cortisol by the adrenal glands. Pituitary adenomas are responsible for 80% of endogenous Cushing's syndrome, when excluding Cushing's syndrome from exogenously administered corticosteroids. The equine version of this disease is Pituitary pars intermedia dysfunction.
Congenital adrenal hyperplasia (CAH) is a group of autosomal recessive disorders characterized by impaired cortisol synthesis. It results from the deficiency of one of the five enzymes required for the synthesis of cortisol in the adrenal cortex. Most of these disorders involve excessive or deficient production of hormones such as glucocorticoids, mineralocorticoids, or sex steroids, and can alter development of primary or secondary sex characteristics in some affected infants, children, or adults. It is one of the most common autosomal recessive disorders in humans.
Hydrocortisone is the name for the hormone cortisol when supplied as a medication. Uses include conditions such as adrenocortical insufficiency, adrenogenital syndrome, high blood calcium, thyroiditis, rheumatoid arthritis, dermatitis, asthma, and COPD. It is the treatment of choice for adrenocortical insufficiency. It can be given by mouth, topically, or by injection. Stopping treatment after long-term use should be done slowly.
Glucocorticoids are a class of corticosteroids, which are a class of steroid hormones. Glucocorticoids are corticosteroids that bind to the glucocorticoid receptor that is present in almost every vertebrate animal cell. The name "glucocorticoid" is a portmanteau and is composed from its role in regulation of glucose metabolism, synthesis in the adrenal cortex, and its steroidal structure.
Adrenal insufficiency is a condition in which the adrenal glands do not produce adequate amounts of steroid hormones. The adrenal glands—also referred to as the adrenal cortex—normally secrete glucocorticoids, mineralocorticoids, and androgens. These hormones are important in regulating blood pressure, electrolytes, and metabolism as a whole. Deficiency of these hormones leads to symptoms ranging from abdominal pain, vomiting, muscle weakness and fatigue, low blood pressure, depression, mood and personality changes to organ failure and shock. Adrenal crisis may occur if a person having adrenal insufficiency experiences stresses, such as an accident, injury, surgery, or severe infection; this is a life-threatening medical condition resulting from severe deficiency of cortisol in the body. Death may quickly follow.
Lipoid congenital adrenal hyperplasia is an endocrine disorder that is an uncommon and potentially lethal form of congenital adrenal hyperplasia (CAH). It arises from defects in the earliest stages of steroid hormone synthesis: the transport of cholesterol into the mitochondria and the conversion of cholesterol to pregnenolone—the first step in the synthesis of all steroid hormones. Lipoid CAH causes mineralocorticoid deficiency in affected infants and children. Male infants are severely undervirilized causing their external genitalia to look feminine. The adrenals are large and filled with lipid globules derived from cholesterol.
Congenital adrenal hyperplasia due to 21-hydroxylase deficiency (CAH) is a genetic disorder characterized by impaired production of cortisol in the adrenal glands.
Hypoaldosteronism is an endocrinological disorder characterized by decreased levels of the hormone aldosterone. Similarly, isolated hypoaldosteronism is the condition of having lowered aldosterone without corresponding changes in cortisol.
Adrenalectomy is the surgical removal of one or both adrenal glands. It is usually done to remove tumors of the adrenal glands that are producing excess hormones or is large in size. Adrenalectomy can also be done to remove a cancerous tumor of the adrenal glands, or cancer that has spread from another location, such as the kidney or lung. Adrenalectomy is not performed on those who have severe coagulopathy or whose heart and lungs are too weak to undergo surgery. The procedure can be performed using an open incision (laparotomy) or minimally invasive laparoscopic or robot-assisted techniques. Minimally invasive techniques are increasingly the gold standard of care due to shorter length of stay in the hospital, lower blood loss, and similar complication rates.
Adrenocorticotropic hormone deficiency is a rare disorder characterized by secondary adrenal insufficiency with minimal or no cortisol production and normal pituitary hormone secretion apart from ACTH. ACTH deficiency may be congenital or acquired, and its symptoms are clinically similar to those of glucocorticoid deficiency. Symptoms consist of weight loss, diminished appetite, muscle weakness, nausea, vomiting, and hypotension. Low blood sugar and hyponatremia are possible; however, blood potassium levels typically remain normal because affected patients are deficient in glucocorticoids rather than mineralocorticoids because of their intact renin-angiotensin-aldosterone system. ACTH may be undetectable in blood tests, and cortisol is abnormally low. Glucocorticoid replacement therapy is required. With the exception of stressful situations, some patients with mild or nearly asymptomatic disease may not require glucocorticoid replacement therapy. As of 2008 about two hundred cases have been described in the literature.
The ACTH test is a medical test usually requested and interpreted by endocrinologists to assess the functioning of the adrenal glands' stress response by measuring the adrenal response to adrenocorticotropic hormone or another corticotropic agent such as tetracosactide or alsactide (Synchrodyn). ACTH is a hormone produced in the anterior pituitary gland that stimulates the adrenal glands to release cortisol, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), and aldosterone.
Critical illness–related corticosteroid insufficiency is a form of adrenal insufficiency in critically ill patients who have blood corticosteroid levels which are inadequate for the severe stress response they experience. Combined with decreased glucocorticoid receptor sensitivity and tissue response to corticosteroids, this adrenal insufficiency constitutes a negative prognostic factor for intensive care patients.
Hypoadrenocorticism in dogs, or, as it is known in people, Addison's disease, is an endocrine system disorder that occurs when the adrenal glands fail to produce enough hormones for normal function. The adrenal glands secrete glucocorticoids such as cortisol and mineralocorticoids such as aldosterone; when proper amounts of these are not produced, the metabolic and electrolyte balance is upset. Mineralocorticoids control the amount of potassium, sodium, and water in the body. Hypoadrenocorticism is fatal if left untreated.
Adrenal gland disorders are conditions that interfere with the normal functioning of the adrenal glands. Your body produces too much or too little of one or more hormones when you have an adrenal gland dysfunction. The type of issue you have and the degree to which it affects your body's hormone levels determine the symptoms.
Glucocorticoid deficiency is a condition where the body doesn’t produce enough glucocorticoid hormones.
Late onset congenital adrenal hyperplasia (LOCAH), also known as nonclassic congenital adrenal hyperplasia, is a milder form of congenital adrenal hyperplasia (CAH), a group of autosomal recessive disorders characterized by impaired cortisol synthesis that leads to variable degrees of postnatal androgen excess.
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