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Adrenal Gland Diseases

1
Agenda
Addisons Disease
Cushings Syndrome
Pheochromocytoma

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Addisons Disease
resulting in inadequate production of glucocorticoid and mineralocorticoid
Addison disease, or primary adrenal insufficiency, is a
chronic disorder of the adrenal cortex
an annual incidence about 4 per million in Western populations
It is a relatively rare disease with a prevalence of about 140
per million and
yet its diagnosis is often missed or delayed
Addison disease is a potentially lethal condition if left
untreated
have a perception of reduced health-related quality of life and remain at risk
of premature death
Furthermore, recent studies have shown that treated
patients with Addison disease
Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.
3
Causes of Addisons Disease
Autoimmunity
Autoimmune polyendocrinopathy syndrome type 1
Autoimmune polyendocrinopathy syndrome type 2
Isolated autoimmune Addison disease
Infective
Tuberculosis
Fungal
AIDS
Genetic
Adrenoleukodystrophy
Congenital adrenal hyperplasia
Adrenal hypoplasia congenital
Familial glucocorticoid deficiency
IMAGe syndrome
Allgrove syndrome (Triple A syndrome)
Kearns-Sayre syndrome (Mitochondrial Addison disease)

Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.

4
Causes of Addisons Disease (Contd..)
Miscellaneous
Infiltration
Hemorrhage
Infarction
Iatrogenic

Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.

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Symptoms, Signs and Investigations that Point to
Addisons Disease
*Late manifestations of the disease
**Cardinal sign of Addison disease
Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.


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Symptoms Signs Laboratory results
Fatigue
Malaise
Loss of appetite
Nausea and vomiting
Abdominal pain
Weight loss
Postural dizziness*
Funny turns may be
due to postural
hypotension or
hypoglycemia*
Myalgia
Joint pain
Salt craving
Loss of libido
(particularly in women)
Hyperpigmentation of
skin and mucous
membranes**
Low blood pressure
Postural hypotension*
Hyponatremia
Hyperkalemia
Hypoglycaemia
Raised urea
Metabolic acidosis
Hypercalcemia
Raised thyroid-
stimulating hormone
Normocytic anemia
Diagnosing Addisons Disease
A morning serum cortisol level higher than 500 nmol/L (18 g/dL) usually
excludes Addison disease
while a level below 165 nmol/L (6 g/dL) is suggestive of adrenal insufficiency
However, most patients will need a short synacthen test for confirmation or
exclusion of Addison disease
This involves injecting 250 g of synacthen (tetracosactrin; synthetic
analogue of ACTH) IM or IV
Blood samples for serum cortisol are taken at 0, 30, and 60 minutes
An increase in serum cortisol level 30 or 60 minutes after synacthen injection
to above 500 nmol/L (18 g/dL) is considered a normal response
although the threshold cortisol level may vary according to local laboratory reference ranges


Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.


7
Diagnosing Addisons Disease (Contd..)
If the cortisol response to synacthen is inadequate,
plasma ACTH level should be measured
patients with secondary adrenal insufficiency due to pituitary or
hypothalamic disorders have a low or inappropriately normal
plasma ACTH level
A raised plasma ACTH level confirms the diagnosis of
Addison disease, whereas
is sometimes a useful investigation to distinguish between Addison
disease and secondary adrenal insufficiency
Plasma renin activity is elevated in Addison disease
and


Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.


8
Algorithm to Determine the Cause of Addisons Disease
in Adults



Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.



9
APS1 autoimmune polyendocrinopathy syndrome type 1; APS2 autoimmune polyendocrinopathy
syndrome type 2; PTH parathyroid hormone; VLCFA very long-chain fatty acid.
Management of Addisons Disease
Routine treatment of Addison disease involves
replacement of the glucocorticoid and mineralocorticoid
hormones

Some forms of Addison disease also will require specific
treatment for the underlying cause
for example, antituberculous drugs in Addison disease due to
tuberculosis

Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.

10
Management of Addisons Disease: Glucocorticoid
Replacement
Hydrocortisone is most commonly used for glucocorticoid
replacement
although other glucocorticoids, including cortisone, prednisolone, and
dexamethasone are occasionally used
Long-acting glucocorticoids, dexamethasone, and prednisolone
have the advantage of a once-daily dosing schedule
but have the drawback of losing the diurnal pattern, resulting in excess
glucocorticoid levels overnight
In Addison disease, standard replacement dose of hydrocortisone is
15-25 mg a day, given in 2 or 3 divided doses
A typical starting regime consists of hydrocortisone 10 mg on
waking, 5 mg at around noon, and 5 mg early evening

Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.

11
Management of Addisons Disease: Glucocorticoid
Replacement (Contd..)
There are no satisfactory biochemical tests to assess the
adequacy of glucocorticoid replacement

In practice, the dose of hydrocortisone is maintained on
the basis of clinical assessment taking an account of
patients wellbeing, and
presence of any signs of over-replacement (eg, hypertension,
weight gain, thin skin, easy bruising, and glucose intolerance)
or
under-replacement (eg, weight loss and pigmentation)
12

Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.

Management of Addisons Disease: Glucocorticoid
Replacement (Contd..)
During intercurrent illnesses, perioperative periods, and
other forms of stress
patients should increase the dose of hydrocortisone to mimic
the normal physiological response

Some drugs (eg, rifampicin, phenobarbitone, and
phenytoin) increase hepatic metabolism of
glucocorticoids, and
patients starting on such drugs may need to increase the dose
of hydrocortisone
13

Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.

Management of Addisons Disease: Glucocorticoid
Replacement (Contd..)
Recommendations for an Increased Dose Hydrocortisone in Patients with
Addison Disease in Different Conditions
14

Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.

*No need to replace mineralocorticoid at these doses of hydrocortisone as high dose hydrocortisone has mineralocorticoid activity.
Management of Addisons Disease: Mineralocorticoid
Replacement
Fludrocortisone is the only available agent for mineralocorticoid replacement
The usual starting dose is 100 g a day
The dose is adjusted (usually 50-200 g a day) according to clinical response
Hypertension and presence of ankle edema suggest over-replacement
Salt craving, postural hypotension, and hyperkalemia are signs of under-
replacement
An assessment of plasma renin activity also is helpful in optimizing the dose of
fludrocortisone
Suppressed and elevated plasma renin activity indicate over-replacement and
under-replacement, respectively
15

Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.

Management of Addisons Disease: Patient Education
Patient education is critical for the successful
management of Addison disease

Information on management of steroid replacement
during sickness can prevent acute adrenal crisis

Patients should carry a steroid card and a medic alert
bracelet with details of the diagnosis

They and their family members should be taught to give
intramuscular hydrocortisone injections during
emergencies

Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.

16
Management of Addisons Disease: Follow-up
to assess well-being,
monitor whether the glucocorticoid and mineralocorticoid
replacement is adequate, and
reinforce patient education
Patients with Addisons disease should be reviewed
annually
with full blood count (pernicious anemia), fasting glucose (diabetes
mellitus), and serum thyrotropin (thyroid dysfunction), and check
the regularity of menstrual cycle in women (premature ovarian
failure)
In patients with autoimmune Addisons disease,
screening should be done annually for associated
autoimmune disorders

Chakera AJ, Vaidya B. Addison Disease in Adults: Diagnosis and Management. The American Journal of Medicine. 2010; 123:
409 413.

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Cushings Syndrome
Cushings syndrome is caused by excessive activation of
glucocorticoid receptors

By far the most common cause is iatrogenic
due to prolonged administration of synthetic glucocorticoids
such as prednisolone

Non-iatrogenic Cushings syndrome is rare and
is often a spot diagnosis made by an astute clinician

Strachan MWJ, Walker BR. Endocrine Disease. In: Colledge NR, Walker BR, Ralston HS, eds. Davidsons Principles and Practice
of Medicine. 21
st
ed. Edinburgh: Elsevier; 2010: 768.

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Classification/Etiology of Cushings syndrome
ACTH-dependent
Pituitary adenoma secreting ACTH (Cushings disease)
Ectopic ACTH syndrome (bronchial carcinoid, small-cell lung carcinoma, other
neuroendocrine tumour)
Iatrogenic (ACTH therapy)
Non-ACTH-dependent
Iatrogenic (chronic glucocorticoid therapy)
Adrenal adenoma
Adrenal carcinoma
Pseudo-Cushings syndrome*
Alcohol excess (biochemical and clinical features)
Major depressive illness (biochemical features only, some clinical overlap)
Primary obesity (mild biochemical features, some clinical overlap)
19

Strachan MWJ, Walker BR. Endocrine Disease. In: Colledge NR, Walker BR, Ralston HS, eds. Davidsons Principles and Practice
of Medicine. 21
st
ed. Edinburgh: Elsevier; 2010: 768.

*Cortisol excess as part of another illness.
Clinical Manifestations of Cushings Syndrome
20

Strachan MWJ, Walker BR. Endocrine Disease. In: Colledge NR, Walker BR, Ralston HS, eds. Davidsons Principles and Practice
of Medicine. 21
st
ed. Edinburgh: Elsevier; 2010: 768.

Algorithm for Management of Patient with Suspected
Cushing's Syndrome
CHR, corticotropin-releasing hormone; DEX, dexamethasone.
Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
Edition:
www.accessmedicine.com

21
Diagnostic Tests to Determine the Type of Cushings
Syndrome



Adamson JW, Longo DL. Anemia and Polycythemia. In: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson
JL, eds. Harrisons Principles of Internal Medicine. 16th ed. New York, NY: McGraw-Hill; 2005: 330.



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Treatment of Cushing's Syndrome
Treatment consists of surgical removal of the adrenal tumor
For smaller tumors - a minimally invasive approach preferred
For larger tumors and those suspected of malignancy, an open
approach is preferred
ACTH-independent disease:
Treatment of choice is selective removal of pituitary corticotrope
tumor, usually via a transsphenoidal approach
Long-term follow-up is important as late relapse occurs in a
significant number of patients
If pituitary disease recurs, options include second surgery,
radiotherapy, stereotactic radiosurgery, and bilateral adrenalectomy
These options need to be applied in a highly individualized fashion
Cushing's disease:

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
Edition:
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Treatment of Cushing's Syndrome (Contd..)
it may be necessary to introduce medical therapy to rapidly control the
cortisol excess during the period leading up to surgery
In some with very severe, overt Cushing's (e.g. difficult to
control hypokalemic hypertension or acute psychosis)
long-term antiglucocorticoid drug treatment may be required
In patients with metastasized, glucocorticoid-producing
carcinomas
one must carefully weigh whether drug treatment or bilateral
adrenalectomy is the most appropriate choice
The latter facilitates immediate cure but require life-long corticosteroid
replacement
In this instance, it is paramount to ensure regular imaging follow-up for
identification of the ectopic ACTH source
In case of ectopic ACTH syndrome (in which the tumor
cannot be located)
24


Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
Edition:
www.accessmedicine.com


Treatment of Cushing's Syndrome (Contd..)
Metyrapone inhibits cortisol synthesis at the level of 11 -hydroxylase
Antimycotic drug ketoconazole inhibits the early steps of steroidogenesis
Typical starting doses are 500 mg/tid for metyrapone (maximum dose, 6 g)
and 200 mg/tid for ketoconazole (maximum dose, 1200 mg)
Oral agents with established efficacy in Cushing's syndrome
are metyrapone and ketoconazole
because of its side effect profile, it is most commonly used in the context of
adrenocortical carcinoma
but, low-dose treatment (5001000 mg per day) has also been used in
benign Cushing's
Mitotane, a derivative of the insecticide o,p'DDD, is an
adrenolytic agent that is also effective for reducing cortisol
It is administered by continuous IV infusion in low, nonanesthetic doses
In severe cases of cortisol excess, etomidate can be used to
lower cortisol

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
Edition:
www.accessmedicine.com

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Treatment of Cushing's Syndrome (Contd..)
After the successful removal of an ACTH- or cortisol-
producing tumor, the HPA axis will remain suppressed
Thus, hydrocortisone replacement needs to be initiated at the
time of surgery and slowly tapered following recovery, to
allow physiologic adaptation to normal cortisol levels

Depending on degree and duration of cortisol excess,
the HPA axis may require many months or even years to
resume normal function

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
Edition:
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Pheochromocytoma
derived from the sympathetic or parasympathetic nervous system
Pheochromocytomas and paragangliomas are
catecholamine-producing tumors
features of multiple endocrine neoplasia type 2 or several other
pheochromocytoma-associated syndromes
These tumors may arise sporadically or be inherited as
their removal can prevent hypertensive crises that can be lethal
Diagnosis of pheochromocytomas provides a potentially
correctable cause of hypertension, and
to a patient in hypertensive crisis with associated cerebrovascular or cardiac
complications
The clinical presentation is variable, ranging from an
adrenal incidentaloma

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
Edition:
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27

Epidemiology of Pheochromocytoma

Pheochromocytoma is estimated to occur in 28 of 1 million persons per year,
and about 0.1% of hypertensive patients harbor a pheochromocytoma
Autopsy series reveal prevalence of 0.2%
The mean age at diagnosis is about 40 years, although the tumors can occur
from early childhood until late in life
The "rule of tens" for pheochromocytomas states that about 10% are bilateral,
10% are extraadrenal, and 10% are malignant
However, these percentages are higher in the inherited syndromes

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
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Etiology and Pathogenesis of Pheochromocytoma

that arise from cells derived from the sympathetic (e.g. adrenal medulla) or
parasympathetic (e.g. carotid body, glomus vagale) paraganglia
Pheochromocytomas and paragangliomas are well-
vascularized tumors
caused by chromaffin oxidation of catecholamines
The name pheochromocytoma reflects the black-colored
staining
including those in extraadrenal retroperitoneal, pelvic, and thoracic sites
Most clinicians use the term pheochromocytoma to
describe symptomatic catecholamine-producing tumors
The term paraganglioma is used to describe
catecholamine-producing tumors in the head and neck
These tumors may secrete little or no catecholamines

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
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29

Etiology and Pathogenesis of Pheochromocytoma
(Contd..)

The etiology of sporadic pheochromocytomas and paragangliomas
is unknown
including germ-line mutations in the RET, VHL, NF1, SDHB, SDHC, SDHD, or
SDHAF2 genes
However, about 25% of patients have an inherited condition
RET mutations activate the receptor tyrosine kinase activity
Biallelic gene inactivation has been demonstrated for the VHL,
NF1, and SDH genes, whereas
SDH is an enzyme of the Krebs cycle and the mitochondrial
respiratory chain
VHL mutations reduce protein degradation, resulting in upregulation of components
involved in cell cycle progression, glucose metabolism, and oxygen sensing
The VHL protein is a component of a ubiquitin E3 ligase

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
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Clinical Features Associated with Pheochromocytoma


Headaches
Sweating attacks
Palpitations and tachycardia
Hypertension, sustained or paroxysmal
Anxiety and panic attacks
Pallor
Nausea
Abdominal pain
Weakness
Weight loss
Paradoxical response to antihypertensive drugs
Polyuria and polydipsia
Constipation
Orthostatic hypotension
Dilated cardiomyopathy
Erythrocytosis
Elevated blood sugar
Hypercalcemia

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
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Diagnosis of Pheochromocytoma


Pheochromocytomas and paragangliomas synthesize
and store catecholamines
which include norepinephrine (noradrenaline), epinephrine
(adrenaline), and dopamine

Elevated plasma and urinary levels of catecholamines
and the methylated metabolites, metanephrines, are
the cornerstone for the diagnosis

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
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Biochemical and Imaging Methods Used for
Pheochromocytoma and Paraganglioma Diagnosis

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
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Diagnostic Method Sensitivity Specificity
24-h urinary tests
Vanillylmandelic acid ++ ++++
Catecholamines +++ +++
Fractionated metanephrines ++++ ++
Total metanephrines +++ ++++
Plasma tests
Catecholamines +++ ++
Free metanephrines ++++ +++
CT ++++ +++
MRI ++++ +++
MIBG scintigraphy +++ ++++
Somatostatin receptor scintigraphy
*
++ ++
Dopa (dopamine) PET +++ ++++
*
Particularly high in head and neck paragangliomas.
Abbreviations: MIBG, metaiodobenzylguanidine; PET, positron emission tomography.
Diagnostic Imaging for Pheochromocytoma
A variety of methods have been used to localize
pheochromocytomas and paragangliomas

CT and MRI are similar in sensitivity

CT should be performed with contrast

T2-weighted MRI with gadolinium contrast is optimal for
detecting pheochromocytomas and
is somewhat better than CT for imaging extra-adrenal
pheochromocytomas and paragangliomas

About 5% of adrenal incidentalomas, which usually are
detected by CT or MRI
prove to be pheochromocytomas after endocrinologic evaluation

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
Edition:
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34
Diagnostic Imaging for Pheochromocytoma (Contd..)
Tumors also can be localized by using radioactive tracers
including 131I- or 123I-metaiodobenzylguanidine (MIBG),
111In-somatostatin analogues, or 18F-dopa (or dopamine)
positron emission tomography (PET)

Because these agents exhibit selective uptake in
paragangliomas
nuclear imaging is particularly useful in the hereditary
syndromes

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
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35
Differential Diagnosis of Pheochromocytoma
Essential hypertension
Anxiety attacks
Use of cocaine or amphetamines
Mastocytosis or carcinoid syndrome (usually lacking hypertension)
intracranial lesions
Clonidine withdrawal
Autonomic epilepsy, and
Factitious crises (usually from sympathomimetic amines)
When one is entertaining the possibility of a
pheochromocytoma, other disorders to consider include
A nonfunctioning adrenal adenoma
Aldosteronoma, and
Cortisol-producing adenoma (Cushing's syndrome)
When an asymptomatic adrenal mass is identified, likely
diagnoses other than pheochromocytoma include

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
Edition:
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Treatment of Pheochromocytoma
Complete tumor removal is the ultimate therapeutic goal
Preoperative patient preparation is essential for safe surgery
-Adrenergic blockers (phenoxybenzamine) should be initiated at relatively low doses
(e.g., 510 mg orally 3 times per day) and increased as tolerated every few days
Because patients are volume-constricted, liberal salt intake and hydration are
necessary to avoid orthostasis
Adequate alpha blockade generally requires 7 days, with a typical final dose of 2030
mg phenoxybenzamine three times per day
Oral prazosin or intravenous phentolamine can be used to manage paroxysms while
awaiting adequate alpha blockade

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
Edition:
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37
Treatment of Pheochromocytoma (Contd..)
Before surgery, blood pressure should be consistently
below 160/90 mmHg, with moderate orthostasis

Beta blockers (e.g. 10 mg propranolol 3 to 4 times per
day) can be added
after starting alpha blockers and increased as needed if
tachycardia persists

Other antihypertensives, such as calcium channel
blockers or angiotensin-converting enzyme inhibitors
have been used when blood pressure is difficult to control
with phenoxybenzamine alone

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
Edition:
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38
Treatment of Pheochromocytoma (Contd..)
Surgery should be performed by teams of anesthesiologists and surgeons with
experience in the management of pheochromocytomas
Blood pressure can be labile during surgery, particularly at the onset of
intubation or when the tumor is manipulated
Nitroprusside infusion is useful for intraoperative hypertensive crises, and
hypotension usually responds to volume infusion
Laparotomy was the traditional surgical approach
Endoscopic surgery, using either a transperitoneal or a retroperitoneal
approach, is associated with fewer complications, a faster recovery, and
optimal cosmetic results

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
Edition:
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39
Treatment of Pheochromocytoma (Contd..)
Atraumatic endoscopic surgery has become the method of choice
It may be possible to preserve the normal adrenal cortex, particularly in
hereditary disorders in which bilateral pheochromocytomas are more likely
Extra-adrenal abdominal as well as most thoracic pheochromocytomas also
can be removed endoscopically
Postoperatively, catecholamine normalization should be documented
An adrenocorticotropic hormone test should be used to exclude cortisol
deficiency when bilateral adrenal cortexsparing surgery is performed

Longo DL., Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Harrisons Principle of Internal Medicine, 18
th
Edition:
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