3. OBJECTIVE
• To be able to promptly identify Addisonian
Crisis and initiate appropraite measures to
save the patient’s life.
• It presents masked like many other
ailments – making prompt identification,
life saving.
4. • Do not confuse acute adrenal crisis with Addison
disease.
• In 1885, Thomas Addison described a syndrome of long
term adrenal insufficiency that develops over months to
years with:
o weakness,
o Fatigue,
o Anorexia,
o Weight loss and hyperpigmentation as the primary
symptoms.
• In contrast, an acute adrenal crisis can manifest with
vomiting, abdominal pain and hypovolemic shock.
Overview
5. Overview
• Hahner et al investigated the frequency and causes of,
as well as the risk factors for, adrenal crisis in patients
with chronic adrenal insufficiency.
• Using a disease-specific questionnaire, the authors
analyzed data from 444 patients, including 254 with
primary adrenal insufficiency and 190 with secondary
adrenal insufficiency.
• At least 1 adrenal crisis was reported by 42% of patients,
including 47% of those with primary adrenal insufficiency
and 35% of patients with the secondary condition.
• GI infection and fever were the most common
precipitating causes of crisis.
• Identified risk factors for adrenal crisis were, for patients
with primary adrenal insufficiency, concomitant
nonendocrine disease and for patients with secondary
adrenal insufficiency, female sex and diabetes
insipidus
6. Lets Paint an Overview Picture
• “Anyone on Prednisolone for long enough
to suppress the PA axis or who has
overwhelming sepsis, or has metastatic
cancer may suddenly develop adrenal
insufficiency with deadly hypovolemic
shock”
7. Epidemiology
• “Addison's disease was frequently consequent upon affectation of
the glands by tuberculosis. Pulmonary Tuberculosis (PTB) is still
very common in Nigeria but no report on the functional status of the
adrenal cortex in patients with PTB in Nigeria exists”
• “Adrenocortical insufficiency, mostly at the subclinical level, is
common in persons with PTB infection, occurring in about 23% of
patients. We therefore recommend that basal cortisol levels should
not be used to detect adrenocortical insufficiency; rather stimulation
tests should be used to exclude or confirm suspected adrenocortical
insufficiency in patients with PTB”.
Odeniyi I.A et al Mar.2011
8. • Studies of critically ill patients with septic shock
demonstrate a de novo (excluding patients with known
adrenal insufficiency or patients on glucocorticoid
therapy) incidence ranging from 19-54%.
• Annane et al's landmark 2002 study found a very high
rate, ie, 76% of all enrolled patients with septic shock
• In a study of 2000 consecutive general hospital
autopsies, only 22 (1.1%) revealed bilateral adrenal
hemorrhage; however, as many as 15% of patients dying
in shock have been demonstrated to have BMAH.
• No description regarding racial data, sexual predilection,
or age is available in the literature.
9. • The prevalence of primary adrenal insufficiency (Addison's disease)
has been reported to be 39 to 60 per million population.
May M. et al
• Most cases in Nigeria due to TB & HIV
Mortality/Morbidity
• In the absence of bilateral adrenal hemorrhage, the survival rate of
patients with acute adrenal crisis that is diagnosed promptly and
treated appropriately approaches that of patients without acute
adrenal crisis with similar severity of illness.
• Patients who developed BMAH before the availability of hormonal
testing or computed tomography (CT) scanning rarely survived. In
one series, patients who were diagnosed using CT scanning had an
85% rate of survival. Because the true incidence of adrenal crisis
and BMAH are unknown, the actual mortality rate also is unknown.
11. Anatomy & Physiology
• Each adrenal gland has two parts
– Adrenal Medulla (inner area)
•Secretes catecholamines which mediate stress
response (help prepare a person for
emergencies).
»Norepinephrine
»Epinephrine
»Dopamine
12. • The adrenal medulla comprises approximately
28% of the total adrenal mass.
• Although we think of the ‘stress’
catecholamines as being necessary for ‘fight
or flight’, they are actually circulating in our
bodies, in minute quantities, at all times, and
act in concert with other hormones and the
vagus nerve to support daily activities.
13. • Adrenal Cortex (outer area, encloses Adrenal Medulla)
– Secretes steroid hormones
• Glucocorticoids (Cortisol): exert a widespread
effect on metabolism of carbohydrates and
proteins
• Mineralocorticoids (Aldosterone, 11-
Deoxycortocosterone): are essential to maintain
sodium and fluid balance
• sex hormones (Androgens: DHEA) secondary
source
14. Interestingly…
• A functioning adrenal cortex (or the steady
availability of replacement hormone) is essential for
survival.
• A person can survive without a functioning adrenal
medulla.
15. Survive without my Medulla?!
• This seems counter-intuitive doesn’t it? You would think we
would need epinephrine/norepinephrine as a critical
component to survive.
• Research has shown that even after the adrenal medulla has
been destroyed by radiation or removal, small amounts of
those catecholamines are found in the body.
• The source is unknown, however the amount is sufficient for
survival.
16. The Essential Steroids
• Primary glucocorticoid:
– Cortisol (a.k.a. hydrocortisone)
• Primary mineralocorticoid:
– Aldosterone
“These steroids, especially cortisol, are essential for
life.”
17.
18.
19.
20. Cortisol
• A glucocorticoid
• Frequently referred to as the ‘stress hormone’
– Released in response to physiological or
psychological stress
•Examples: exercise, illness, injury, starvation,
extreme dehydration, electrolyte imbalance,
emotional stress, surgery, etc.
21. Cortisol
• When cortisol is not produced or released by the
adrenal glands, humans are unable to respond
appropriately to physiologic stressors.
• Rapid deterioration resulting in organ damage and
shock/coma/death can occur, especially in children.
23. Why we need cortisol
• Cortisol has a necessary effect on the vascular
system (blood vessels, heart) and liver during
episodes of physiologic stress
24. Vascular Reactivity
• In adrenally-insufficient individuals experiencing a
physiologic stressor, the vascular smooth muscle will
become non-responsive to the effects of
norepinephrine and epinephrine, resulting in
vasodilation and capillary ‘leaking’.
• The patient may be unable to maintain an adequate
blood pressure
• The blood vessels cannot respond to the stress and
will eventually collapse
25. • This is an important reason why adrenally-
insufficient people must receive emergency cortisol
as soon as possible after a serious stress event such
as trauma or a period of nausea/vomiting.
• The vasculature becomes unable to constrict to
make effective use of circulating body volume.
• Replacement IV fluid challenges often have poor
effect in the adrenally-insufficient patient until
cortisol is administered.
26. Energy Metabolism
• In adrenally-insufficient individuals under increased
physiologic stress, the liver is unable to metabolize
carbohydrates properly, which may result in
profoundly low blood sugar that is difficult to reverse
without administration of replacement cortisol
• Impaired gluconeogenesis, lipolysis and proteolysis
27. • The speed at which patient deterioration
occurs is difficult to predict and is related to
the underlying stressor, patient age, general
health, etc.
• Young children can be at high risk for rapid
deterioration, even when experiencing a
‘simple’ gastrointestinal disorder.
28. • The steroid hormones, especially cortisol, are
mediated by the hypothalamic-pituitary-
adrenal (HPA) axis.
• The onset of stress as well as our sleep/wake
cycles influences the activity of the HPA axis.
29. Endocrinologist Testimony…
• “…In adrenal insufficiency, because of the
inability to produce glucocorticoids and often
mineralocorticoids from the adrenal glands, there
is a risk of life-threatening hyponatremia,
hyperkalemia, hypoglycemia, seizures and
cardiovascular collapse, in particular at times of
physiologic stress to the body, such as in injury
or illness…”
• Support letter, Dr. Christine Leudke, Boston
Children’s Hospital 12/12/2009
30. Who has adrenal insufficiency?
• Anyone whose adrenal glands have stopped producing steroids as a result
of:
– Long-term administration of steroids
– Pituitary gland problems, including growth hormone deficiency,
tumor, etc.
– Trauma, including head trauma that affects pituitary
– Loss of circulation to adrenals/Adrenal Hemorrhage/removal of tissue
– Auto-immune disease
– Surgical Removal(For Cushing's) + Inadequate Replacement Therapy.
– Cancer and other diseases (TB and HIV may cause)
• There is also an inherited form of adrenal insufficiency (CAH)
• Acute Vs. Chronic
32. Parent testimony…
• “… People without adrenal insufficiencies naturally produce up to ten
times the normal amount of cortisol during times of physical stress. If an
unaffected person is unresponsive, goes into cardiac arrest or is vomiting,
you can treat the shock, heart, or dehydration and help them. For James,
however, immediate, appropriate emergency response is vital. I have
watched James, as a fever quickly spiked, go from alert and playful to
grayish-white and lethargic, in a matter of minutes. It is scary. I have
seen how a stress dose of Cortef quickly brought him back to where I
could then manage his illness with the “common” treatment of Motrin
and fluids…”
• Oral Testimony, Alex Dubois, December 12, 2009
33. Adrenal Insufficiency: Take Note of this group of
Pxts.
• Can occur from long-term administration of steroids
(over-rides body’s own steroid production)
Examples:
– Organ transplant patients
– Long-term COPD
– Long-term Asthma
– Severe arthritis
– Certain cancer treatments
34. Organ Transplant Patients
• These individuals must take immunosuppressive
medications (usually steroids) DAILY for life.
• Their own adrenal glands stop producing cortisol
because of external source of steroid.
35. Long-term Asthma and COPD
• These individuals are at high risk of adrenal crisis
from illness or trauma
• Keep in mind that many children and teens with
severe asthma take steroid medication every day
and may be at significant risk of adrenal crisis.
• A severely asthmatic teen may have been started
on a steroid 10+ years ago
36. • In some situations steroids are administered long-term and
then tapered off. Often it can take up to a year for a
person’s own adrenal glands to become fully functioning
again.
• These patients remain at risk of adrenal crisis until such
time.
• Too rapid withdrawal of exogenous steroid may
precipitate adrenal crisis, or sudden stress may induce
cortisol requirements in excess of the adrenal glands'
ability to respond immediately.
• In acute illness, a normal cortisol level may
actually reflect adrenal insufficiency because the
cortisol level should be quite elevated
37. Why?
• Adrenal glands tend to get ‘lazy’ when steroids are
regularly administered by mouth, I.M. injection or
I.V. infusion.
• To illustrate how quickly…Just 4 weeks of daily oral
cortisone administration is sufficient to cause the
adrenals to be slightly less responsive to stressors.
39. Primary Adrenal Insufficiency=
Addison’s Disease
• The adrenal glands are damaged and cannot
produce sufficient steroid
• 80% of the time, damage is caused by an auto-
immune response that destroys the adrenal
cortex
• Addison’s can affect both sexes and all age
groups
40. ADRENAL GLAND (1o
) PITUITARY GLAND (2o
)
Autoimmune idiopathic destruction
•Adrenal cortex alone is affected
•Shows atrophy with lymphocytic infiltration and abnormal T-cell
action directed against it
--20
to hypopituitarism
Destruction of adrenal gland by TB Due to suppression of the HPA axis by exogenous steroids
Destruction by amyloidosis and Hemochromatosis Decreased pituitary ACTH production. Hence with 20
adrenal
insufficiency, no skin hyperpigmentation due to low ACTH and
its precursor POMC.
Infiltration of gland by secondary carcinoma, Hodgkin’s
lymphoma or leukemia
These cases are mostly cortisol deficient. Mineralocorticoid Prod
remains normal.
Hence Hyponatremia and hyperkalemia not common.
Infarction of gland caused by meningococcal septicemia
*WaterHouse Friderischen syndrome*
Hemorrhage destruction from use of anticoagulants or lupus
anticoagulant
CAH and use of drugs which block steroid synthesis e.g
ketoconazole,
41. Congenital Adrenal Hyperplasia
• CAH is inherited (recessive gene, each parent
contributes)
– Diagnosed by newborn screening; prior to successful
screening techniques most children died
– Daily replacement oral hormones are required at a
maintenance dose for LIFE
– I.M. or I.V. hormones necessary for stressors (illness,
surgery, fever, trauma, etc.)
– 21-Hydroxylase Def. Most common. Deficient cortisol and
aldosterone. Excess Androgens. Masucilinization and
occasionally Na loss and AI.
42.
43.
44. Defect Deficient
Hormones
Excess Effects
Desmolase deficiency ALL steroids Cholesterol Accumulation
(lipoid hyperplasia)
• AI
• Disease is seldom
compatible with life
• All affected persons
appear to be phenotypic
females as there is lack of
androgens in affected
males.
3 Beta Hydroxysteroid DH Cortisol & Aldosterone DHEA • Affected patients are
severely cortisol and
aldosterone deficient
• Salt losers
• Males have hypospadias
• Females mild virilism
• Elevated 17 OHCS in urine
11 Beta Hydroxylase Cortisol and aldosterone Androgens
11-deoxycortisol
• Masculinization
• HTN from excess 11-
deoxycorticosterone
• Excretion of 11-
deoxycortisol is raised
17 Hydroxylase Deficiency Androgens and Estrogens
Cortisol
Corticosterone
11-dexoycorticosterone
HTN
Hypokalemia
Alkalosis
Ambiguous genitalia in males
Immature female
18-hydroxylase deficiency Aldosterone corticosterone Salt loss
Elevated plasma renin
No genital anomaly
45. Addison’s symptoms
• This disease has a gradual onset and can be
difficult to diagnose:
– Chronic, worsening fatigue; weak, listless and dehydrated
– Apathy + Mood disorders
– Anorexia, Weight loss
– Muscle weakness, Abdominal pain (unexplained)
– Loss of appetite, Nausea/vomiting
– Hypothermia
– Low blood pressure, Pulse is thready, Postural
Hypotension invariably present
– Low blood sugar
– Skin hyperpigmentation(Palmar, Buccal, Gingival,
skinfolds, pressure points)
– Salt-craving
46. Investigations & Findings For Adrenal
Insufficiency
• Low levels of plasma cortisol; diurnal variation Is lost.
Plasma ACTH is elevated (1o
AI especially).
• A random morning cortisol determination is not sufficient
to make a diagnosis in MILD Adrenal insufficiency since
normal levels overlap with levels found in such pts.
• Morning level of <3ug/dl is suggestive of AI
• The finding of a plasma cortisol level < 20ug/dl in a
PATIENT UNDER STRESS e.g. Hypotensive pt., pt.
under intensive care, suggests Adrenal insufficiency.
• .
47. Investigations & Findings For Adrenal Insufficiency
• FBS: LOW
• Electrolytes: initially normal, later on
1. Low Na+
2. High K+
3. Raised Blood urea
4. Low Hco3
(Na/k <5meq/l)
FBC + ESR
Anemia
Leucopenia with lymphocytosis
Increased eosinophil count
Increased ESR
ECG:
Low voltage complexes
Increased PR (?1o
HB) and QT interval (?Hypocalcaemia)
48. Investigation and Findings
• ACTH STIMULATION TEST
Lack of increase in cortisol secretion by the adrenals to
*tetracosactide/tetracosatrin/synacthen*
SHORT SYNACTHEN
(1/2 Hour screening test)
LONG SYNACTHEN
Measures serum cortisol response to
250ug of synacthen given I.M
Do plasma cortisol before and 1/2 our
after synacthen Test. Exclude
Addison if 2nd cortisol >550nmol/l
Done if short synacthen test
response is flat. Helps distinguish
also primary vs. secondary AI 1mg of
synacthen given IM
Normally: initial level of cortisol
should be >200nmol/l
Normal response: Serum cortisol
should more than double in 1st
hour.
45 min. Post synacthen:
Plasma cortisol level ought to have
risen to 600nmol/l or more
4 hours Post 1mg: conc. Of plasma
cortisol ought to be >1000nmol/l
Values less than above: In keeping
with AI (Primary or secondary)
Primary AI: NO RESPONSE @ all.
Secondary AI: have higher values @
24hrs compared to those @ 4hrs.
49. Investigations and Findings Contd.
• Failure to increase plasma cortisol levels after administration
of ACTH.
• Circulating adrenal auto-antibodies(esp.21-Hydroxylase) in
serum in those with auto-immune forms
• 9AM ACTH levels increased (300ng/l). Low or undetectable
levels of ACTH occurs in those due to pituitary disease
• n/b Falsely elevated Cortisol levels in OCP use, Pregnancy
• Insulin Hypoglycemia test (Insulin Tolerance test)
Used to detect 2o
AI
Can be fatal in those with adrenal failure
0.1 to 0.15U/kg I.V
Cortisol level is determined during period of symptomatic hypoglycemia
Normal response occurs when the peak cortisol level is greater than 20ug/dl
51. Acute manifestation of Addison’s is
called Addison Crisis
• Severe vomiting/diarrhea
• Dehydration
• Hypotension
• Sudden, severe pain in back, belly or legs
• Loss of consciousness
• Can be fatal
52. How Do I recognize it first time?
Relevant clue? See the list below:
•Unexplained shock, usually refractory to
fluid and pressor resuscitation
•Nausea, vomiting, abdominal or flank pain
•Hyperthermia or hypothermia
53. Presentation of Adrenal Crisis
• The patient may present with any illness or
injury as the precipitating event.
• A patient’s history of adrenal insufficiency warrants a careful assessment
under specific protocols
• Children may deteriorate into adrenal crisis from a simple fever, a
gastrointestinal illness, a fall from a bicycle or some other injury.
• A mild illness or injury can easily precipitate an adrenal crisis in any age
group
54. Critical Clinical Presentation
• The early indicators of an adrenal-crisis onset
can be vague and non-specific. Some or all
signs/symptoms may be present.
• Infants:
– Poor appetite
– Vomiting/diarrhea
– Lethargy/unresponsive
• Unexplained hypoglycemia
– Seizure/cardiovascular collapse/death
55. Critical Clinical Presentation
(not all S&S may be present)
Older Children/Adults
• Vomiting
• Hypotensive, often unresponsive to
fluids/pressors
– Pallor, gray, diaphoretic
Hypoglycemia, often refractory to D50
• May have neurologic deficits
– Headache/confusion/seizure
– lethargy/unresponsive
• Cardiovascular collapse
• Death
56. • Clearly, the signs/symptoms of adrenal crisis are
similar to other serious shock-type presentations.
• For these patients, standard shock management
requires supplementation with corticosteroid
medication (Solu-Cortef or Solu-Medrol)
• It is important to ANTICIPATE the evolution of an
adrenal crisis and medicate appropriately under the
specific protocols.
• Do not wait until a full adrenal crisis has developed.
Organ damage or death may result from delays.
57. Outline of Management
• Quick, Brief History (Informant)
• If AC suspected, treat before biochemical
results
• Meanwhile ABC started ASA patient is in
ER.
• IV Cortisol
• IVF
• Monitor blood glucose
• Blood, urine, sputum for culture
• Antibiotics
58. History
• Prior steroid use: @least 20 mg daily of
prednisone or its equivalent for at least 5 days
within the past 12 months..
• Organisms associated with adrenal crisis (e.g.,
Haemophilus influenzae, Staphylococcus aureus,
Streptococcus pneumonia, fungi)
• Meningococcemia
• Severe physiologic stress e.g. sepsis, trauma,
Burns, surgery.
59. History
•Anticoagulants, hemorrhagic diathesis
•Azotemia
•Newborn, complicated pregnancy
•Adrenocorticotropin therapy, known primary or secondary
adrenocortical insufficiency (medic-alert bracelet/necklace, OR by
the child, parent or care provider verbally confirming a history of
adrenal insufficiency).
•AIDS
•Invasive or infiltrative disorders
•Tuberculosis
•Topical steroids: Risk of adrenal crisis occurs when used over a
large surface area for a prolonged duration, using occlusive
dressings and a highly potent drug.
•Inhaled steroids: Use of a high dose (>0.8mg/d) over a
prolonged duration increases risk. Fluticasone may cause
suppression at lower dose.
60. Remember!
It is important to note that you are caring for a
patient with multiple issues:
1. The precipitating event (a trauma/illness that may be
a critical issue on its own)
and
2. The evolution towards adrenal crisis, which will result
in organ failure/death if not reversed.
61. Keep In Mind:
• Administration of steroid medication should come
as soon after appropriate A-B-C assessment and
interventions as possible
• Your emergency management priorities remain the
same, with the addition of steroid administration.
• Should I worry about CUSHINGOID?!
62. Lab Studies.
• Serum chemistry: Abnormalities are present in as many as 56% of patients.
Hyponatremia is common (although not diagnostic); hyperkalemia,
metabolic acidosis, and hypoglycemia also may be present. However, the
absence of laboratory abnormalities does not exclude the diagnosis of
adrenal crisis.
• Serum cortisol: Less than 20 mcg/dL in severe stress or after ACTH
stimulation is indicative of adrenal insufficiency.
• ACTH test (diagnostic): Determine baseline serum cortisol, then administer
ACTH 250 mcg intravenous push (IVP), and then draw serum cortisol 30
and 60 minutes after ACTH administration. An increase of less than 9
mcg/dL is considered diagnostic of adrenal insufficiency.
• CBC: Anemia (mild and nonspecific), lymphocytosis, and eosinophilia
(highly suggestive) may be present.
• Serum thyroid levels: Assess for autoimmune, infiltrative, or multiple
endocrine disorders.
• Cultures: Perform blood and other cultures as clinically indicated. Infection
is a common cause of acute adrenal crisis.
63. Imaging Studies: CXR (TB, Histoplasmosis, malignant disease,
sarcoid and lymphoma)
Abdominal CT Scan: Visualize for hemorrhage, atrophy, infiltrative
disorders and metastatic disease.
Adrenal
hemorrhage
appears as
hyperdense,
bilaterally enlarged
adrenal gland
64. BMAH
• Bilateral massive adrenal Hemorrhage
occurs (BMAH) occurs under severe
physiologic stress e.g.
1.Myocardial infarction
2.Septic shock
3.Complicated pregnancy
4.Concomitant coagulopathy or
thromboembolic disorders
65. Others
Electrocardiography
•Prolongation of the QT interval can induce ventricular arrhythmias.
•Deep negative T waves have been described in acute adrenal crisis.
Histology
•Depends on the cause of the adrenal failure.
• In primary adrenocortical failure, histologic evidence of infection,
infiltrative disease, or other condition may be demonstrated.
•Secondary adrenocortical insufficiency may cause atrophy of the
adrenals or no histologic evidence at all, especially if due to exogenous
steroid ingestion.
•Appearance of bilateral adrenal hemorrhage may be striking, as if
bags of blood are replacing the glands.
66. Rx.
Administration of glucocorticoids (+/- Mineralocorticoid) in
supraphysiologic or stress doses is the only definitive therapy.
•Dexamethasone does not interfere with serum cortisol assay
and, thus, may be the initial drug of choice. However, because
dexamethasone has little mineralocorticoid activity, fluid and
electrolyte replacement are essential.
•A short ACTH stimulation test may be performed during
resuscitation. Once complete, hydrocortisone 100 mg IV every 6
hours is the preferred treatment to provide mineralocorticoid
support.
•Delaying glucocorticoid replacement therapy while awaiting the
results of the ACTH stimulation test is inappropriate and
dangerous.
67. Rx Protocol Updates
• Adults
“For patients with confirmed adrenal insufficiency, give
hydrocortisone 100 mg IV, IM or IO OR
methylprednisolone 125 mg IV, IM or IO”
• Pediatric
“For patients with confirmed adrenal insufficiency, give
hydrocortisone 2mg/kg to maximum 100 mg IV, IM
or IO OR methylprednisolone 2mg/kg to maximum
125 mg IV, IM or IO”
68. Rx.
• In addition to corticosteroid replacement, aggressive fluid
replacement with 5% or 10% intravenous dextrose and
saline solutions and treatment of hyperkalemia is
mandatory.
• Fludrocortisone, a mineralocorticoid, may also be given.
Dose of 50-300mcg
• A thorough search for a precipitating cause and
administration of empiric antibiotics is indicated.
Reversal of coagulopathy should be attempted with fresh
frozen plasma.
• Pressors (eg, dopamine, norepinephrine) may be
necessary to combat hypotension.
70. Patient’s Own Medication
• Many adrenally-insufficient patients carry an
emergency Act-O-Vial of Solu-Cortef.
• Solu-Cortef is included in the required
medication formulary, making it acceptable
for paramedics to administer the patient’s
own medication to the patient or to assist the
patient in administering his/her own Solu-
Cortef.
71. Profile: Solu-Cortef
Trade name: Solu-Cortef
Generic name: hydrocortisone sodium succinate
Class: corticosteroid, Pregnancy Class C
Mechanism: acts to suppress inflammation;
Replaces absent glucocorticoids,
acts to suppress immune response
73. Additional Notes
• This product contains the preservative Benzyl
Alcohol in negligible amounts which is found
in many medications.
• The exception is the newly-born and/or
significantly underweight neonates. In these
groups there is insufficient data; this
medication may cause ‘gasping syndrome’,
therefore use in this age-range is not
recommended for pre-hospital setting
74. Additional Notes
• Solu-Cortef is the first choice for management of
adrenal insufficiency/adrenal crisis.
• The other approved medication, Solu-Medrol, is an
acceptable alternative choice for specific
management of adrenal insufficiency/adrenal crisis
75. Why Solu-Cortef > Solu-Medrol
• Solucortef is preferred because essentially it is
a replacement form of the missing hormone,
cortisol. It has both a corticosteroid and a
mineralocorticoid effect.
• Solu-Medrol also has a corticosteroid effect,
but does not provide the mineralocorticoid
action. In an emergency setting, it is an
acceptable alternative to Solu-Cortef.
76. Drug Class Summary
Dexamethasone (Decadron, Baldex, Dexone)
•Used as empiric treatment of shock in suspected adrenal
crisis or insufficiency until serum cortisol levels are drawn.
Hydrocortisone (Hydrocortone, Hydrocort, SoluCortef)
• DOC because of mineralocorticoid activity and
glucocorticoid effects.
Cortisone (Cortone)
•Oral DOC for patients with adrenocortical insufficiency.
•Use in patients undergoing moderate stress surgery (eg,
vascular bypass, total joint replacement) who can take PO
postoperatively.
77. Fludrocortisone (Florinef)
•Acts on renal distal tubules to enhance reabsorption of sodium.
•Increases urinary excretion of both potassium and hydrogen
ions.
•The consequence of these 3 primary effects, together with
similar actions on cation transport in other tissues, appears to
account for the spectrum of physiological activities characteristic
of mineralocorticoids.
•Used in adrenal insufficiency. Produces marked sodium
retention and increased urinary potassium excretion.
Methylprednisolone (Medrol, Solu-Medrol, Depo-Medrol)
•Usually third-line DOC for adrenal crisis because of lack of
mineralocorticoid activity.
•Consider use in patients with fluid overload, edema, or
hypokalemia.
79. Prognosis
• Prognosis is the same as for patients
without adrenal insufficiency if the
condition is diagnosed and treated
appropriately.
80. Resources
• CARES Foundation (www.caresfoundation.org)
• Review of Medical Physiology 17th
edition. Ganong, William F., Appleton &
Lange
• Prescribing Information, Solu-Cortef, Sept 2009 Pharmacia & Upjohn (division
of Pfizer)
• Prescribing information, Solu-Medrol, 2009, Pfizer
• MA Statewide Treatment Protocols, version 8.03
• “Management of Adrenal Crisis, How Should Glucocorticoids Be
Administered?” Stanhope, et al, Journal of Pediatric Endocrinology Vol 16,
Issue 8 pp 99-100
• “Mortality in Canadian Children with Growth Hormone Deficiency Receiving
GH Therapy 1967-1992” Taback, et al, Journal of Clinical Endocrinology &
Metabolism Vol 81, #5 pp 1693-1696
• Adrenal Crisis: Lisa Kirkland, MD, FACP, FCCM, MSHA;
